Glutamate is the precursor for the synthesis of GABA.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

The tuberoinfundibular pathway links the hypothalamus with the pituitary gland, rather than the pineal gland.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

A fenestrated cavum septum pellucidum is linked to dementia pugilistica.

Dementia Pugilistica: A Neurodegenerative Condition Resulting from Neurotrauma

Dementia pugilistica, also known as chronic traumatic encephalopathy (CTE), is a neurodegenerative condition that results from neurotrauma. It is commonly seen in boxers and NFL players, but can also occur in anyone with neurotrauma. The condition is characterized by symptoms such as gait ataxia, slurred speech, impaired hearing, tremors, disequilibrium, neurobehavioral disturbances, and progressive cognitive decline.

Most cases of dementia pugilistica present with early onset cognitive deficits, and behavioral signs exhibited by patients include aggression, suspiciousness, paranoia, childishness, hypersexuality, depression, and restlessness. The progression of the condition leads to more prominent behavioral symptoms such as difficulty with impulse control, irritability, inappropriateness, and explosive outbursts of aggression.

Neuropathological abnormalities have been identified in CTE, with the most unique feature being the abnormal accumulation of tau in neurons and glia in an irregular, focal, perivascular distribution and at the depths of cortical sulci. Abnormalities of the septum pellucidum, such as cavum and fenestration, are also a common feature.

While the condition has become increasingly rare due to the progressive improvement in sports safety, it is important to recognize the potential long-term consequences of repeated head injuries and take steps to prevent them.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Frontal lobe damage can be best detected through tests of verbal fluency, such as the FAS Verbal Fluency Test, as the anterior cerebral artery supplies the frontal lobes and medial aspects of the parietal and occipital lobes, which are responsible for this function.

Parietal Lobe Dysfunction: Types and Symptoms

The parietal lobe is a part of the brain that plays a crucial role in processing sensory information and integrating it with other cognitive functions. Dysfunction in this area can lead to various symptoms, depending on the location and extent of the damage.

Dominant parietal lobe dysfunction, often caused by a stroke, can result in Gerstmann’s syndrome, which includes finger agnosia, dyscalculia, dysgraphia, and right-left disorientation. Non-dominant parietal lobe dysfunction, on the other hand, can cause anosognosia, dressing apraxia, spatial neglect, and constructional apraxia.

Bilateral damage to the parieto-occipital lobes, a rare condition, can lead to Balint’s syndrome, which is characterized by oculomotor apraxia, optic ataxia, and simultanagnosia. These symptoms can affect a person’s ability to shift gaze, interact with objects, and perceive multiple objects at once.

In summary, parietal lobe dysfunction can manifest in various ways, and understanding the specific symptoms can help diagnose and treat the underlying condition.

Cerebrovascular accidents (CVA), also known as strokes, are defined by the World Health Organization as a sudden onset of focal neurological symptoms lasting more than 24 hours and presumed to be of vascular origin. Strokes can be caused by either infarction of hemorrhage, with infarction being more common. Hemorrhagic strokes tend to be more severe. Intracranial hemorrhage can be primary, caused mainly by hypertension, of subarachnoid, caused by the rupture of an aneurysm of angioma. Primary intracranial hemorrhage is most common in individuals aged 60-80 and often occurs during exertion. Infarction can be caused by thrombosis of embolism, with thrombosis being more common. Atherosclerosis, often caused by hypertension, is the main cause of infarction. CT scanning is the preferred diagnostic tool during the first 48 hours after a stroke as it can distinguish between infarcts and hemorrhages. Recovery from embolism is generally quicker and more complete than from thrombosis due to the availability of collateral channels.

Understanding the Blood Brain Barrier

The blood brain barrier (BBB) is a crucial component of the brain’s defense system against harmful chemicals and ion imbalances. It is a semi-permeable membrane formed by tight junctions of endothelial cells in the brain’s capillaries, which separates the blood from the cerebrospinal fluid. However, certain areas of the BBB, known as circumventricular organs, are fenestrated to allow neurosecretory products to enter the blood.

When it comes to MRCPsych questions, the focus is on the following aspects of the BBB: the tight junctions between endothelial cells, the ease with which lipid-soluble molecules pass through compared to water-soluble ones, the difficulty large and highly charged molecules face in passing through, the increased permeability of the BBB during inflammation, and the theoretical ability of nasally administered drugs to bypass the BBB.

It is important to remember the specific circumventricular organs where the BBB is fenestrated, including the posterior pituitary and the area postrema. Understanding the BBB’s function and characteristics is essential for medical professionals to diagnose and treat neurological disorders effectively.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

A gyrus is a ridge on the cerebral cortex, and there are several important gyri to be aware of in exams. These include the angular gyrus in the parietal lobe for language, mathematics, and cognition; the cingulate gyrus adjacent to the corpus callosum for emotion, learning, and memory; the fusiform gyrus in the temporal lobe for face and body recognition, as well as word and number recognition; the precentral gyrus in the frontal lobe for voluntary movement control; the postcentral gyrus in the parietal lobe for touch; the lingual gyrus in the occipital lobe for dreaming and word recognition; the superior frontal gyrus in the frontal lobe for laughter and self-awareness; the superior temporal gyrus in the temporal lobe for language and sensation of sound; the parahippocampal gyrus surrounding the hippocampus for memory; and the dentate gyrus in the hippocampus for the formation of episodic memory.

White matter is the cabling that links different parts of the CNS together. There are three types of white matter cables: projection tracts, commissural tracts, and association tracts. Projection tracts connect higher centers of the brain with lower centers, commissural tracts connect the two hemispheres together, and association tracts connect regions of the same hemisphere. Some common tracts include the corticospinal tract, which connects the motor cortex to the brainstem and spinal cord, and the corpus callosum, which is the largest white matter fiber bundle connecting corresponding areas of cortex between the hemispheres. Other tracts include the cingulum, superior and inferior occipitofrontal fasciculi, and the superior and inferior longitudinal fasciculi.

Dysarthria is a speech disorder that affects the volume, rate, tone, of quality of spoken language. There are different types of dysarthria, each with its own set of features, associated conditions, and localisation. The types of dysarthria include spastic, flaccid, hypokinetic, hyperkinetic, and ataxic.

Spastic dysarthria is characterised by explosive and forceful speech at a slow rate and is associated with conditions such as pseudobulbar palsy and spastic hemiplegia.

Flaccid dysarthria, on the other hand, is characterised by a breathy, nasal voice and imprecise consonants and is associated with conditions such as myasthenia gravis.

Hypokinetic dysarthria is characterised by slow, quiet speech with a tremor and is associated with conditions such as Parkinson’s disease.

Hyperkinetic dysarthria is characterised by a variable rate, inappropriate stoppages, and a strained quality and is associated with conditions such as Huntington’s disease, Sydenham’s chorea, and tardive dyskinesia.

Finally, ataxic dysarthria is characterised by rapid, monopitched, and slurred speech and is associated with conditions such as Friedreich’s ataxia and alcohol abuse. The localisation of each type of dysarthria varies, with spastic and flaccid dysarthria affecting the upper and lower motor neurons, respectively, and hypokinetic, hyperkinetic, and ataxic dysarthria affecting the extrapyramidal and cerebellar regions of the brain.

Cerebral Asymmetry in Planum Temporale and its Implications in Language and Auditory Processing

The planum temporale, a triangular region in the posterior superior temporal gyrus, is a highly lateralized brain structure involved in language and music processing. Studies have shown that the planum temporale is up to ten times larger in the left cerebral hemisphere than the right, with this asymmetry being more prominent in men. This asymmetry can be observed in gestation and is present in up to 70% of right-handed individuals.

Recent research suggests that the planum temporale also plays an important role in auditory processing, specifically in representing the location of sounds in space. However, reduced planum temporale asymmetry has been observed in individuals with dyslexia, stuttering, and schizophrenia. These findings highlight the importance of cerebral asymmetry in the planum temporale and its implications in language and auditory processing.

Catecholamines are a group of chemical compounds that have a distinct structure consisting of a benzene ring with two hydroxyl groups, an intermediate ethyl chain, and a terminal amine group. These compounds play an important role in the body and are involved in various physiological processes. The three main catecholamines found in the body are dopamine, adrenaline, and noradrenaline. All of these compounds are derived from the amino acid tyrosine. Overall, catecholamines are essential for maintaining proper bodily functions and are involved in a wide range of physiological processes.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Abnormal movements known as athetoid movements are commonly associated with issues in the basal ganglia.

Cerebellar Dysfunction: Symptoms and Signs

Cerebellar dysfunction is a condition that affects the cerebellum, a part of the brain responsible for coordinating movement and balance. The symptoms and signs of cerebellar dysfunction include ataxia, intention tremor, nystagmus, broad-based gait, slurred speech, dysdiadochokinesis, and dysmetria (lack of finger-nose coordination).

Ataxia refers to the lack of coordination of voluntary movements, resulting in unsteady gait, difficulty with balance, and clumsiness. Intention tremor is a type of tremor that occurs during voluntary movements, such as reaching for an object. Nystagmus is an involuntary movement of the eyes, characterized by rapid, jerky movements.

Broad-based gait refers to a wide stance while walking, which is often seen in individuals with cerebellar dysfunction. Slurred speech, also known as dysarthria, is a common symptom of cerebellar dysfunction, which affects the ability to articulate words clearly. Dysdiadochokinesis is the inability to perform rapid alternating movements, such as tapping the fingers on the palm of the hand.

Dysmetria refers to the inability to accurately judge the distance and direction of movements, resulting in errors in reaching for objects of touching the nose with the finger. These symptoms and signs of cerebellar dysfunction can be caused by a variety of conditions, including stroke, multiple sclerosis, and alcoholism. Treatment depends on the underlying cause and may include medications, physical therapy, and surgery.

Motor Neuron Lesions

Signs of an upper motor neuron lesion include weakness, increased reflexes, increased tone (spasticity), mild atrophy, an upgoing plantar response (Babinski reflex), and clonus. On the other hand, signs of a lower motor neuron lesion include atrophy, weakness, fasciculations, decreased reflexes, and decreased tone. It is important to differentiate between the two types of lesions as they have different underlying causes and require different treatment approaches. A thorough neurological examination can help identify the location and extent of the lesion, which can guide further diagnostic testing and management.

Myelin sheaths are composed of cells containing fat that act as insulation for the axons of neurons. These cells run along the axons with gaps between them called nodes of Ranvier. The fat in the myelin sheath makes it a poor conductor, causing impulses to jump from one gap to the next, which increases the speed of transmission of action potentials.

The white matter of the brain gets its whitish appearance from the myelin sheath, which is made up of glial cells. Oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system are responsible for forming the myelin sheath. The electrical impulse jumps from one node to the next at a rapid rate of up to 120 meters per second, which is known as saltatory conduction.

Glycoproteins play a crucial role in the formation, maintenance, and degradation of myelin sheaths. Recent studies suggest that dysfunction in oligodendrocytes and myelin can lead to changes in synaptic formation and function, resulting in cognitive dysfunction, a core symptom of schizophrenia. Additionally, there is evidence linking oligodendrocyte and myelin dysfunction with abnormalities in dopamine and glutamate, both of which are found in schizophrenia. Addressing these abnormalities could offer therapeutic opportunities for individuals with schizophrenia.

The enzyme choline acetyltransferase facilitates the production of acetylcholine by catalyzing the combination of choline and Acetyl coenzyme A.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Hirano bodies are a nonspecific indication of neurodegeneration and are primarily observed in.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Mirror Neurons: A Model for Imitation Learning

Mirror neurons are a unique type of visuomotor neurons that were first identified in the premotor cortex of monkeys in area F5. These neurons fire not only when the monkey performs a specific action but also when it observes another individual, whether it is a monkey of a human, performing a similar action. This discovery has led to the development of a model for understanding imitation learning.

Mirror neurons offer a fascinating insight into how humans and animals learn by imitation. They provide a neural mechanism that allows individuals to understand the actions of others and to replicate those actions themselves. This process is essential for social learning, as it enables individuals to learn from others and to adapt to their environment.

The discovery of mirror neurons has also led to new research in the field of neuroscience, as scientists seek to understand how these neurons work and how they can be used to improve our understanding of human behavior. As we continue to learn more about mirror neurons, we may be able to develop new therapies for individuals with social and communication disorders, such as autism.

Overall, mirror neurons are a fascinating area of research that has the potential to revolutionize our understanding of human behavior and learning. By studying these neurons, we may be able to unlock new insights into how we learn, communicate, and interact with others.

Agnosia is a condition where a person loses the ability to recognize objects, persons, sounds, shapes, of smells, despite having no significant memory loss of defective senses. There are different types of agnosia, such as prosopagnosia (inability to recognize familiar faces), anosognosia (inability to recognize one’s own condition/illness), autotopagnosia (inability to orient parts of the body), phonagnosia (inability to recognize familiar voices), simultanagnosia (inability to appreciate two objects in the visual field at the same time), and astereoagnosia (inability to recognize objects by touch).

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Neurofibrillary tangles and neuritic (senile) plaques are commonly found in the brains of elderly individuals, but they are not present in Lewy body dementia. Pick’s disease is characterized by the presence of Pick’s bodies and knife blade atrophy. Creutzfeldt-Jakob disease (CJD) is identified by the spongy appearance of the grey matter in the cerebral cortex due to multiple vacuoles. If an individual experiences short-term memory problems that affect their daily life, it may indicate the presence of dementia. Alzheimer’s disease is characterized by extensive tangles and plaques in the brain.

Brain Anatomy

The brain is a complex organ with various regions responsible for different functions. The major areas of the cerebrum (telencephalon) include the frontal lobe, parietal lobe, occipital lobe, temporal lobe, insula, corpus callosum, fornix, anterior commissure, and striatum. The cerebrum is responsible for complex learning, language acquisition, visual and auditory processing, memory, and emotion processing.

The diencephalon includes the thalamus, hypothalamus and pituitary, pineal gland, and mammillary body. The thalamus is a major relay point and processing center for all sensory impulses (excluding olfaction). The hypothalamus and pituitary are involved in homeostasis and hormone release. The pineal gland secretes melatonin to regulate circadian rhythms. The mammillary body is a relay point involved in memory.

The cerebellum is primarily concerned with movement and has two major hemispheres with an outer cortex made up of gray matter and an inner region of white matter. The cerebellum provides precise timing and appropriate patterns of skeletal muscle contraction for smooth, coordinated movements and agility needed for daily life.

The brainstem includes the substantia nigra, which is involved in controlling and regulating activities of the motor and premotor cortical areas for smooth voluntary movements, eye movement, reward seeking, the pleasurable effects of substance misuse, and learning.

The vulnerability of microglia to HIV infection is highest among all the cell types in the brain. This is because the CD4 and CCR5 receptors required for HIV cell entry are expressed in both parenchymal microglia and perivascular microglia/macrophages. Although there have been some reports of HIV infection in endothelial cells, neurons, and oligodendrocytes, it is generally accepted that such infections are rare and unlikely to play a significant role in HIV-related CNS disorders. Astrocytes are thought to be capable of only a limited form of HIV infection.

Understanding Action Potentials in Neurons and Muscle Cells

The membrane potential is a crucial aspect of cell physiology, and it exists across the plasma membrane of most cells. However, in neurons and muscle cells, this membrane potential can change over time. When a cell is not stimulated, it is in a resting state, and the inside of the cell is negatively charged compared to the outside. This resting membrane potential is typically around -70mV, and it is maintained by the Na/K pump, which maintains a high concentration of Na outside and K inside the cell.

To trigger an action potential, the membrane potential must be raised to around -55mV. This can occur when a neurotransmitter binds to the postsynaptic neuron and opens some ion channels. Once the membrane potential reaches -55mV, a cascade of events is initiated, leading to the opening of a large number of Na channels and causing the cell to depolarize. As the membrane potential reaches around +40 mV, the Na channels close, and the K gates open, allowing K to flood out of the cell and causing the membrane potential to fall back down. This process is irreversible and is critical for the transmission of signals in neurons and the contraction of muscle cells.

Brain Blood Supply and Consequences of Occlusion

The brain receives blood supply from the internal carotid and vertebral arteries, which form the circle of Willis. The circle of Willis acts as a shunt system in case of vessel damage. The three main vessels arising from the circle are the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Occlusion of these vessels can result in various neurological deficits. ACA occlusion may cause hemiparesis of the contralateral foot and leg, sensory loss, and frontal signs. MCA occlusion is the most common and can lead to hemiparesis, dysphasia/aphasia, neglect, and visual field defects. PCA occlusion may cause alexia, loss of sensation, hemianopia, prosopagnosia, and cranial nerve defects. It is important to recognize these consequences to provide appropriate treatment.

Brain Blood Supply and Consequences of Occlusion

The brain receives blood supply from the internal carotid and vertebral arteries, which form the circle of Willis. The circle of Willis acts as a shunt system in case of vessel damage. The three main vessels arising from the circle are the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Occlusion of these vessels can result in various neurological deficits. ACA occlusion may cause hemiparesis of the contralateral foot and leg, sensory loss, and frontal signs. MCA occlusion is the most common and can lead to hemiparesis, dysphasia/aphasia, neglect, and visual field defects. PCA occlusion may cause alexia, loss of sensation, hemianopia, prosopagnosia, and cranial nerve defects. It is important to recognize these consequences to provide appropriate treatment.

Broca’s and Wernicke’s are two types of expressive dysphasia, which is characterized by difficulty producing speech despite intact comprehension. Dysarthria is a type of expressive dysphasia caused by damage to the speech production apparatus, while Broca’s aphasia is caused by damage to the area of the brain responsible for speech production, specifically Broca’s area located in Brodmann areas 44 and 45. On the other hand, Wernicke’s aphasia is a type of receptive of fluent aphasia caused by damage to the comprehension of speech, while the actual production of speech remains normal. Wernicke’s area is located in the posterior part of the superior temporal gyrus in the dominant hemisphere, within Brodmann area 22.

Serotonin (5-hydroxytryptamine, 5-HT) receptors are primarily G protein receptors, except for 5-HT3, which is a ligand-gated receptor. It is important to remember that 5-HT3 is most commonly associated with nausea. Additionally, 5-HT7 is linked to circadian rhythms. The stimulation of 5-HT2 receptors is believed to be responsible for the side effects of insomnia, agitation, and sexual dysfunction that are associated with the use of selective serotonin reuptake inhibitors (SSRIs).

The strongest association with HIV dementia is the infiltration of monocytes and activation of microglia in the brain. While the presence of HIV encephalopathy is somewhat linked to HIV associated dementia, the extent of monocyte infiltration and microglial activation is the best indicator of AIDS dementia. Microglia can cause damage to neurons by releasing oxidative radicals, nitric oxide, and cytokines. The correlation between viral load and HAD is not significant. Astrocytes have limited susceptibility to HIV infection, and neuronal infection is rare and unlikely to have a significant impact on HIV-related CNS disorders.

Lewy bodies are not exclusively indicative of a particular disease, as they can also be present in individuals with Alzheimer’s and even in those who do not exhibit any noticeable symptoms.

Parkinson’s Disease Pathology

Parkinson’s disease is a neurodegenerative disorder that affects the central nervous system. The pathology of Parkinson’s disease is very similar to that of Lewy body dementia. The macroscopic features of Parkinson’s disease include pallor of the substantia nigra (midbrain) and locus coeruleus (pons). The microscopic changes include the presence of Lewy bodies, which are intracellular aggregates of alpha-synuclein. Additionally, there is a loss of dopaminergic cells from the substantia nigra pars compacta. These changes contribute to the motor symptoms of Parkinson’s disease, such as tremors, rigidity, and bradykinesia. Understanding the pathology of Parkinson’s disease is crucial for developing effective treatments and improving the quality of life for those affected by this condition.

Primary Afferent Axons: Conveying Information about Touch and Pain

Primary afferent axons play a crucial role in conveying information about touch and pain from the surface of the body to the spinal cord and brain. These axons can be classified into four types based on their functions: A-alpha (proprioception), A-beta (touch), A-delta (pain and temperature), and C (pain, temperature, and itch). While all A axons are myelinated, C fibers are unmyelinated.

A-delta fibers are responsible for the sharp initial pain, while C fibers are responsible for the slow, dull, longer-lasting second pain. Understanding the different types of primary afferent axons and their functions is essential in diagnosing and treating various sensory disorders.

The use of HAART has led to a complete elimination of new cases of toxoplasmosis in individuals who are HIV positive. Studies conducted on the Edinburgh cohort have revealed a significant decrease in the occurrence of CMV by 50% during autopsy, a 68% reduction in HIVE, and complete eradication of toxoplasmosis. However, there has been a slight increase in the incidence of PML and lymphoma in this group and other samples.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

EEG Waveform Frequencies

Delta waves have the lowest frequency among the EEG waveforms, ranging from 0.5 to 4 Hz. Theta waves follow with a frequency range of 4 to 8 Hz, while alpha waves have a frequency range of 8 to 14 Hz. Beta waves have a frequency range of 14 to 32 Hz, and gamma waves have a frequency range of 32 to 48+ Hz. In a normal awake adult EEG, alpha waves are the most prominent waveform.

Dementia Pugilistica: A Neurodegenerative Condition Resulting from Neurotrauma

Dementia pugilistica, also known as chronic traumatic encephalopathy (CTE), is a neurodegenerative condition that results from neurotrauma. It is commonly seen in boxers and NFL players, but can also occur in anyone with neurotrauma. The condition is characterized by symptoms such as gait ataxia, slurred speech, impaired hearing, tremors, disequilibrium, neurobehavioral disturbances, and progressive cognitive decline.

Most cases of dementia pugilistica present with early onset cognitive deficits, and behavioral signs exhibited by patients include aggression, suspiciousness, paranoia, childishness, hypersexuality, depression, and restlessness. The progression of the condition leads to more prominent behavioral symptoms such as difficulty with impulse control, irritability, inappropriateness, and explosive outbursts of aggression.

Neuropathological abnormalities have been identified in CTE, with the most unique feature being the abnormal accumulation of tau in neurons and glia in an irregular, focal, perivascular distribution and at the depths of cortical sulci. Abnormalities of the septum pellucidum, such as cavum and fenestration, are also a common feature.

While the condition has become increasingly rare due to the progressive improvement in sports safety, it is important to recognize the potential long-term consequences of repeated head injuries and take steps to prevent them.

Nitric Oxide and Depression

Recent research has indicated that nitric oxide (NO) may play a role in the development of depression. Inhibitors of NO synthase have been found to exhibit antidepressant-like effects in preclinical studies, suggesting that NO may be involved in the pathogenesis of depression. These findings suggest that targeting NO signaling pathways may be a potential therapeutic approach for treating depression. Further research is needed to fully understand the role of NO in depression and to develop effective treatments based on this knowledge.

This question is presented in two variations on the exam, with one implying that auras are primarily linked to temporal lobe epilepsy and the other to complex partial seizures. In reality, partial seizures are most commonly associated with auras compared to other types of seizures. While partial seizures can originate in any lobe of the brain, those that arise in the temporal lobe are most likely to produce an aura. Therefore, both versions of the question are accurate.

Epilepsy and Aura

An aura is a subjective sensation that is a type of simple partial seizure. It typically lasts only a few seconds and can help identify the site of cortical onset. There are eight recognized types of auras, including somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic.

In about 80% of cases, auras precede temporal lobe seizures. The most common auras in these seizures are abdominal and psychic, which can cause a rising epigastric sensation of feelings of fear, déjà vu, of jamais vu. Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type, such as an electrical sensation of tingling. Occipital lobe seizures may begin with contralateral visual changes, such as colored lines, spots, of shapes, of even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.

Complex partial seizures are defined by impairment of consciousness, which means decreased responsiveness and awareness of oneself and surroundings. During a complex partial seizure, a patient is unresponsive and does not remember events that occurred.

Psychosis is associated with heightened dopaminergic activity in the striatum, while negative symptoms are linked to reduced dopaminergic activity in the frontal lobe.

The Dopamine Hypothesis is a theory that suggests that dopamine and dopaminergic mechanisms are central to schizophrenia. This hypothesis was developed based on observations that antipsychotic drugs provide at least some degree of D2-type dopamine receptor blockade and that it is possible to induce a psychotic episode in healthy subjects with pharmacological dopamine agonists. The hypothesis was further strengthened by the finding that antipsychotic drugs’ clinical effectiveness was directly related to their affinity for dopamine receptors. Initially, the belief was that the problem related to an excess of dopamine in the brain. However, later studies showed that the relationship between hypofrontality and low cerebrospinal fluid (CSF) dopamine metabolite levels indicates low frontal dopamine levels. Thus, there was a move from a one-sided dopamine hypothesis explaining all facets of schizophrenia to a regionally specific prefrontal hypodopaminergia and a subcortical hyperdopaminergia. In summary, psychosis appears to result from excessive dopamine activity in the striatum, while the negative symptoms seen in schizophrenia appear to result from too little dopamine activity in the frontal lobe. Antipsychotic medications appear to help by countering the effects of increased dopamine by blocking postsynaptic D2 receptors in the striatum.

Medial temporal lobe atrophy (MTA) is prevalent in 80% to 90% of individuals diagnosed with Alzheimer’s dementia, and can also be present in other forms of dementia, albeit less frequently and severely. MTA is an early and relatively reliable indicator of Alzheimer’s disease, although it is not exclusive to this condition.

Brain Anatomy

The brain is a complex organ with various regions responsible for different functions. The major areas of the cerebrum (telencephalon) include the frontal lobe, parietal lobe, occipital lobe, temporal lobe, insula, corpus callosum, fornix, anterior commissure, and striatum. The cerebrum is responsible for complex learning, language acquisition, visual and auditory processing, memory, and emotion processing.

The diencephalon includes the thalamus, hypothalamus and pituitary, pineal gland, and mammillary body. The thalamus is a major relay point and processing center for all sensory impulses (excluding olfaction). The hypothalamus and pituitary are involved in homeostasis and hormone release. The pineal gland secretes melatonin to regulate circadian rhythms. The mammillary body is a relay point involved in memory.

The cerebellum is primarily concerned with movement and has two major hemispheres with an outer cortex made up of gray matter and an inner region of white matter. The cerebellum provides precise timing and appropriate patterns of skeletal muscle contraction for smooth, coordinated movements and agility needed for daily life.

The brainstem includes the substantia nigra, which is involved in controlling and regulating activities of the motor and premotor cortical areas for smooth voluntary movements, eye movement, reward seeking, the pleasurable effects of substance misuse, and learning.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Cranial Nerve Reflexes

When it comes to questions on cranial nerve reflexes, it is important to match the reflex to the nerves involved. Here are some examples:

– Pupillary light reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Accommodation reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Jaw jerk: involves the trigeminal nerve (sensory and motor).
– Corneal reflex: involves the trigeminal nerve (sensory) and facial nerve (motor).
– Vestibulo-ocular reflex: involves the vestibulocochlear nerve (sensory) and oculomotor, trochlear, and abducent nerves (motor).

Another example of a cranial nerve reflex is the gag reflex, which involves the glossopharyngeal nerve (sensory) and the vagus nerve (motor). This reflex is important for protecting the airway from foreign objects of substances that may trigger a gag reflex. It is also used as a diagnostic tool to assess the function of these nerves.

Cerebrospinal Fluid: Formation, Circulation, and Composition

Cerebrospinal fluid (CSF) is produced by ependymal cells in the choroid plexus of the lateral, third, and fourth ventricles. It is constantly reabsorbed, so only a small amount is present at any given time. CSF occupies the space between the arachnoid and pia mater and passes through various foramina and aqueducts to reach the subarachnoid space and spinal cord. It is then reabsorbed by the arachnoid villi and enters the dural venous sinuses.

The normal intracerebral pressure (ICP) is 5 to 15 mmHg, and the rate of formation of CSF is constant. The composition of CSF is similar to that of brain extracellular fluid (ECF) but different from plasma. CSF has a higher pCO2, lower pH, lower protein content, lower glucose concentration, higher chloride and magnesium concentration, and very low cholesterol content. The concentration of calcium and potassium is lower, while the concentration of sodium is unchanged.

CSF fulfills the role of returning interstitial fluid and protein to the circulation since there are no lymphatic channels in the brain. The blood-brain barrier separates CSF from blood, and only lipid-soluble substances can easily cross this barrier, maintaining the compositional differences.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

White matter is the cabling that links different parts of the CNS together. There are three types of white matter cables: projection tracts, commissural tracts, and association tracts. Projection tracts connect higher centers of the brain with lower centers, commissural tracts connect the two hemispheres together, and association tracts connect regions of the same hemisphere. Some common tracts include the corticospinal tract, which connects the motor cortex to the brainstem and spinal cord, and the corpus callosum, which is the largest white matter fiber bundle connecting corresponding areas of cortex between the hemispheres. Other tracts include the cingulum, superior and inferior occipitofrontal fasciculi, and the superior and inferior longitudinal fasciculi.

Cerebral Tumours

The most common brain tumours in adults, listed in order of frequency, are metastatic tumours, glioblastoma multiforme, anaplastic astrocytoma, and meningioma. On the other hand, the most common brain tumours in children, listed in order of frequency, are astrocytoma, medulloblastoma, and ependymoma.

Dhat is a syndrome that is specific to Indian culture and affects men. Those who suffer from it experience anxiety about the presence of semen in their urine, which they believe leads to a loss of energy.

Creutzfeldt-Jakob Disease: Differences between vCJD and CJD

Creutzfeldt-Jakob Disease (CJD) is a prion disease that includes scrapie, BSE, and Kuru. However, there are important differences between sporadic (also known as classic) CJD and variant CJD. The table below summarizes these differences.

vCJD:
– Longer duration from onset of symptoms to death (a year of more)
– Presents with psychiatric and behavioral symptoms before neurological symptoms
– MRI shows pulvinar sign
– EEG shows generalized slowing
– Originates from infected meat products
– Affects younger people (age 25-30)

CJD:
– Shorter duration from onset of symptoms to death (a few months)
– Presents with neurological symptoms
– MRI shows bilateral anterior basal ganglia high signal
– EEG shows biphasic and triphasic waves 1-2 per second
– Originates from genetic mutation (bad luck)
– Affects older people (age 55-65)

Overall, understanding the differences between vCJD and CJD is important for diagnosis and treatment.

Agnosia is a condition where a person loses the ability to recognize objects, persons, sounds, shapes, of smells, despite having no significant memory loss of defective senses. There are different types of agnosia, such as prosopagnosia (inability to recognize familiar faces), anosognosia (inability to recognize one’s own condition/illness), autotopagnosia (inability to orient parts of the body), phonagnosia (inability to recognize familiar voices), simultanagnosia (inability to appreciate two objects in the visual field at the same time), and astereoagnosia (inability to recognize objects by touch).

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Cranial Fossae and Foramina

The cranium is divided into three regions known as fossae, each housing different cranial lobes. The anterior cranial fossa contains the frontal lobes and includes the frontal and ethmoid bones, as well as the lesser wing of the sphenoid. The middle cranial fossa contains the temporal lobes and includes the greater wing of the sphenoid, sella turcica, and most of the temporal bones. The posterior cranial fossa contains the occipital lobes, cerebellum, and medulla and includes the occipital bone.

There are several foramina in the skull that allow for the passage of various structures. The most important foramina likely to appear in exams are listed below:

– Foramen spinosum: located in the middle fossa and allows for the passage of the middle meningeal artery.
– Foramen ovale: located in the middle fossa and allows for the passage of the mandibular division of the trigeminal nerve.
– Foramen lacerum: located in the middle fossa and allows for the passage of the small meningeal branches of the ascending pharyngeal artery and emissary veins from the cavernous sinus.
– Foramen magnum: located in the posterior fossa and allows for the passage of the spinal cord.
– Jugular foramen: located in the posterior fossa and allows for the passage of cranial nerves IX, X, and XI.

Understanding the location and function of these foramina is essential for medical professionals, as they play a crucial role in the diagnosis and treatment of various neurological conditions.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Prion Diseases

Prion diseases are a group of rare and fatal neurodegenerative disorders that affect humans and animals. These diseases are caused by abnormal proteins called prions, which can cause normal proteins in the brain to fold abnormally and form clumps. This leads to damage and death of brain cells, resulting in a range of symptoms such as dementia, movement disorders, and behavioral changes.

Some of the most well-known prion diseases in humans include Creutzfeldt-Jakob disease, Kuru, Gerstman-Straussler-Scheinker syndrome, and Fatal Familial Insomnia. Creutzfeldt-Jakob disease is the most common prion disease in humans, and it can occur sporadically, genetically, of through exposure to contaminated tissue. Kuru is a rare disease that was once prevalent in Papua New Guinea, and it was transmitted through cannibalism. Gerstman-Straussler-Scheinker syndrome is a rare genetic disorder that affects the nervous system, while Fatal Familial Insomnia is a rare inherited disorder that causes progressive insomnia and other neurological symptoms.

Despite extensive research, there is currently no cure for prion diseases, and treatment is mainly supportive. Prevention measures include avoiding exposure to contaminated tissue and practicing good hygiene.

Cholecystokinin (CCK) is a hormone produced and released by the duodenum that stimulates the secretion of digestive enzymes and bile, while also acting as an appetite suppressant. corticotropin releasing hormone is secreted by the paraventricular nucleus of the hypothalamus and triggers the release of ACTH from the pituitary gland. Met- and Leu- encephalin are peptides that play a role in pain modulation. α-endorphin is one of several endorphins that can inhibit pain and induce a feeling of euphoria.

Source: https://www.ncbi.nlm.nih.gov/pubmed/16246215

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Gliosis is a discovery that can only be observed under a microscope.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Lesions of the vagus nerve commonly result in the following symptoms: a raspy of weak voice, difficulty swallowing, absence of the gag reflex, deviation of the uvula away from the affected side, and an inability to elevate the palate.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Delta waves are typically observed during stages III and IV of deep sleep and their presence outside of these stages can indicate diffuse slowing and encephalopathy.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Periods of hypersomnia and altered behavior are characteristic of Kleine-Levin syndrome.

Kluver-Bucy Syndrome: Causes and Symptoms

Kluver-Bucy syndrome is a neurological disorder that results from bilateral medial temporal lobe dysfunction, particularly in the amygdala. This condition is characterized by a range of symptoms, including hyperorality (a tendency to explore objects with the mouth), hypersexuality, docility, visual agnosia, and dietary changes.

The most common causes of Kluver-Bucy syndrome include herpes, late-stage Alzheimer’s disease, frontotemporal dementia, trauma, and bilateral temporal lobe infarction. In some cases, the condition may be reversible with treatment, but in others, it may be permanent and require ongoing management. If you of someone you know is experiencing symptoms of Kluver-Bucy syndrome, it is important to seek medical attention promptly to determine the underlying cause and develop an appropriate treatment plan.

Kluver-Bucy Syndrome: Causes and Symptoms

Kluver-Bucy syndrome is a neurological disorder that results from bilateral medial temporal lobe dysfunction, particularly in the amygdala. This condition is characterized by a range of symptoms, including hyperorality (a tendency to explore objects with the mouth), hypersexuality, docility, visual agnosia, and dietary changes.

The most common causes of Kluver-Bucy syndrome include herpes, late-stage Alzheimer’s disease, frontotemporal dementia, trauma, and bilateral temporal lobe infarction. In some cases, the condition may be reversible with treatment, but in others, it may be permanent and require ongoing management. If you of someone you know is experiencing symptoms of Kluver-Bucy syndrome, it is important to seek medical attention promptly to determine the underlying cause and develop an appropriate treatment plan.

The middle cerebral artery is the most frequent location for cerebral infarction, resulting in contralateral paralysis and sensory loss. If the dominant hemisphere is affected, language impairment such as Broca’s of Wernicke’s aphasia may occur. Bilateral anterior cerebellar artery blockage is uncommon but can lead to akinetic mutism, which is characterized by a loss of speech and movement. Non-dominant middle cerebral artery blockage can cause contralateral neglect, as well as motor and sensory dysfunction, but language is typically unaffected. The occlusion of the posterior inferior cerebellar artery can result in lateral medullary syndrome, also known as Wallenberg syndrome, which is characterized by crossed contralateral and trunk sensory deficits and ipsilateral sensory deficits affecting the face and cranial nerves. Emboli in the ophthalmic artery can cause temporary vision loss, also known as amaurosis fugax, which is more commonly caused by emboli originating in the carotid artery.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Night terrors typically occur during deep sleep in stage 4. Upon waking, there is no memory of the experience. These episodes can be considered a dissociative state and may involve automatic behaviors. In some cases, violent behavior may occur during night terrors, but the individual cannot be held accountable for their actions. Family history is not a common factor in the occurrence of night terrors.

If a patient is unable to complete a task that requires a sequence of steps, they are exhibiting ideational apraxia. On the other hand, if they struggle to perform a task that they have previously learned, such as attempting to brush their teeth with a pencil, this is an example of ideomotor apraxia.

Apraxia: Understanding the Inability to Carry Out Learned Voluntary Movements

Apraxia is a neurological condition that affects a person’s ability to carry out learned voluntary movements. It is important to note that this condition assumes that everything works and the person is not paralyzed. There are different types of apraxia, each with its own set of symptoms and characteristics.

Limb kinetic apraxia is a type of apraxia that affects a person’s ability to make fine of delicate movements. This can include tasks such as buttoning a shirt of tying shoelaces.

Ideomotor apraxia, on the other hand, is an inability to carry out learned tasks when given the necessary objects. For example, a person with ideomotor apraxia may try to write with a hairbrush instead of using it to brush their hair.

Constructional apraxia affects a person’s ability to copy a picture of combine parts of something to form a whole. This can include tasks such as building a puzzle of drawing a picture.

Ideational apraxia is an inability to follow a sequence of actions in the correct order. For example, a person with ideational apraxia may struggle to take a match out of a box and strike it with their left hand.

Finally, oculomotor apraxia affects a person’s ability to control eye movements. This can make it difficult for them to track moving objects of read smoothly.

Overall, apraxia can have a significant impact on a person’s ability to carry out everyday tasks. However, with the right support and treatment, many people with apraxia are able to improve their abilities and maintain their independence.

Cannabis attaches to cannabinoid receptors, while heroin acts as an opioid agonist and alters the function of dopamine.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

During REM sleep, the EEG patterns resemble those observed during wakefulness, characterized by numerous beta-rhythms that are fast.

Sleep Stages

Sleep is divided into two distinct states called rapid eye movement (REM) and non-rapid eye movement (NREM). NREM is subdivided into four stages.

Sleep stage
Approx % of time spent in stage
EEG findings
Comment

I
5%
Theta waves (4-7 Hz)
The dozing off stage. Characterized by hypnic jerks: spontaneous myoclonic contractions associated with a sensation of twitching of falling.

II
45%
Theta waves, K complexes and sleep spindles (short bursts of 12-14 Hz activity)
Body enters a more subdued state including a drop in temperature, relaxed muscles, and slowed breathing and heart rate. At the same time, brain waves show a new pattern and eye movement stops.

III
15%
Delta waves (0-4 Hz)
Deepest stage of sleep (high waking threshold). The length of stage 3 decreases over the course of the night.

IV
15%
Mixed, predominantly beta
High dream activity.

The percentage of REM sleep decreases with age.

It takes the average person 15-20 minutes to fall asleep, this is called sleep latency (characterised by the onset of stage I sleep). Once asleep one descends through stages I-II and then III-IV (deep stages). After about 90 minutes of sleep one enters REM. The rest of the sleep comprises of cycles through the stages. As the sleep progresses the periods of REM become greater and the periods of NREM become less. During an average night’s sleep one spends 25% of the sleep in REM and 75% in NREM.

REM sleep has certain characteristics that separate it from NREM

Characteristics of REM sleep

– Autonomic instability (variability in heart rate, respiratory rate, and BP)
– Loss of muscle tone
– Dreaming
– Rapid eye movements
– Penile erection

Deafness:

(No information provided on deafness in relation to sleep stages)

The prion protein has two forms: the normal form (PrPc) and the infectious form (PrPSc). The normal form can be broken down by proteases, while the infectious form is resistant to proteases.

Prion Protein and its Role in Disease

Prion protein is a type of infective agent that is composed of protein. It is made up of proteins called PrP, which exist in two forms: a normal form (PrPC) and an abnormal form (PrPSc). The abnormal form is resistant to protease, which means it cannot be broken down in the body. This abnormal form can change adjacent normal PrPC into the abnormal form, which is how the infection spreads.

PrPC is a normal component of cell membranes and has an alpha-helical structure. However, in PrPSc, much of the alpha-helical structure is replaced by a beta-sheet structure. This change in structure causes PrPSc to aggregate into plaques in the extracellular space of the central nervous system, disrupting normal tissue structure.

Prions cause disease by this disruption of normal tissue structure, leading to neurological symptoms and ultimately death. Understanding the structure and behavior of prion proteins is crucial in developing treatments and preventative measures for prion diseases.

Choline, which is essential for the synthesis of the neurotransmitter acetylcholine, can be obtained in significant quantities from vegetables, seeds, egg yolk, and liver. However, it is only present in small amounts in most fruits, egg whites, and many beverages.

Sleep is a complex process that involves different stages. These stages are categorized into Non-REM (NREM) and Rapid Eye Movement (REM) sleep. Each cycle of NREM and REM sleep takes around 90 to 110 minutes.

Stage 1 is the lightest stage of sleep, where the sleeper may experience sudden muscle contractions and a sense of falling. The brain waves during this stage are called theta waves.

In Stage 2, eye movement stops, and brain waves become lower. Sleep spindles and K complexes, which are rapid bursts of 12-14 Hz waves, are seen during this stage.

Stages 3 and 4 are referred to as deep sleep of delta sleep. There is no eye movement of muscle activity during these stages. Children may experience night terrors of somnambulism during these stages.

REM sleep is characterized by rapid, shallow breathing and rapid, jerky eye movements. Most dreaming occurs during REM sleep.

Overall, the different stages of sleep are important for the body to rest and rejuvenate. Understanding these stages can help individuals improve their sleep quality and overall health.

The EEG findings for Huntington’s disease typically show a widespread decrease in activity with low amplitude theta (θ) and delta (δ) waves. In contrast, CJD is characterized by bilateral, synchronous generalised irregular spike wave complexes occurring at a rate of 1-2/second, often accompanied by myoclonic jerks. Hepatic encephalopathy is associated with widespread slowing and triphasic waves, while herpes simplex encephalitis is linked to repetitive episodic discharges and temporal lobe focal slow waves. HIV typically demonstrates diffuse slowing on EEG.

Anton-Babinski syndrome, also known as Anton syndrome of Anton’s blindness, is a rare condition caused by brain damage in the occipital lobe. Individuals with this syndrome are unable to see due to cortical blindness, but they insist that they can see despite evidence to the contrary. This is because they confabulate, of make up explanations for their inability to see. The syndrome is typically a result of a stroke, but can also occur after a head injury.

The temporal lobe is separated from the frontal and parietal lobes by the Sylvian fissure.

The Cerebral Cortex and Neocortex

The cerebral cortex is the outermost layer of the cerebral hemispheres and is composed of three parts: the archicortex, paleocortex, and neocortex. The neocortex accounts for 90% of the cortex and is involved in higher functions such as thought and language. It is divided into 6-7 layers, with two main cell types: pyramidal cells and nonpyramidal cells. The surface of the neocortex is divided into separate areas, each given a number by Brodmann (e.g. Brodmann’s area 17 is the primary visual cortex). The surface is folded to increase surface area, with grooves called sulci and ridges called gyri. The neocortex is responsible for higher cognitive functions and is essential for human consciousness.

The median raphe nucleus is a group of neurons located in the brainstem that plays a crucial role in regulating mood, anxiety, and stress. It is connected to various brain regions, including the ventral tegmental area (VTA), which is a key component of the brain’s reward system.

The connection between the median raphe nucleus and the VTA is important because it allows for the modulation of reward-related behaviors and emotions. The median raphe nucleus sends serotonergic projections to the VTA, which can influence the release of dopamine, a neurotransmitter that is associated with pleasure and reward.

Studies have shown that disruptions in the communication between the median raphe nucleus and the VTA can lead to various psychiatric disorders, such as depression and addiction. Therefore, understanding the mechanisms underlying this connection is crucial for developing effective treatments for these conditions.

In summary, the connection between the median raphe nucleus and the VTA is an important pathway for regulating reward-related behaviors and emotions, and disruptions in this pathway can lead to psychiatric disorders.

All serotonin receptors, except for 5-HT3, are coupled with G proteins instead of being ligand gated ion channels.

Serotonin (5-hydroxytryptamine, 5-HT) receptors are primarily G protein receptors, except for 5-HT3, which is a ligand-gated receptor. It is important to remember that 5-HT3 is most commonly associated with nausea. Additionally, 5-HT7 is linked to circadian rhythms. The stimulation of 5-HT2 receptors is believed to be responsible for the side effects of insomnia, agitation, and sexual dysfunction that are associated with the use of selective serotonin reuptake inhibitors (SSRIs).

Multisystem Atrophy: A Parkinson Plus Syndrome

Multisystem atrophy is a type of Parkinson plus syndrome that is characterized by three main features: Parkinsonism, autonomic failure, and cerebellar ataxia. It can present in three different ways, including Shy-Drager Syndrome, Striatonigral degeneration, and Olivopontocerebellar atrophy, each with varying degrees of the three main features.

Macroscopic features of multisystem atrophy include pallor of the substantia nigra, greenish discoloration and atrophy of the putamen, and cerebellar atrophy. Microscopic features include the presence of Papp-Lantos bodies, which are alpha-synuclein inclusions found in oligodendrocytes in the substantia nigra, cerebellum, and basal ganglia.

Overall, multisystem atrophy is a complex and debilitating condition that affects multiple systems in the body, leading to a range of symptoms and challenges for patients and their caregivers.

The cortex is composed of neurons, with the majority being pyramidal neurons that are excitatory and contain glutamate. Grey matter is where neural cell bodies are located, while white matter mainly consists of myelinated axon tracts. The color contrast between the two is due to the white appearance of myelin.

The Cerebral Cortex and Neocortex

The cerebral cortex is the outermost layer of the cerebral hemispheres and is composed of three parts: the archicortex, paleocortex, and neocortex. The neocortex accounts for 90% of the cortex and is involved in higher functions such as thought and language. It is divided into 6-7 layers, with two main cell types: pyramidal cells and nonpyramidal cells. The surface of the neocortex is divided into separate areas, each given a number by Brodmann (e.g. Brodmann’s area 17 is the primary visual cortex). The surface is folded to increase surface area, with grooves called sulci and ridges called gyri. The neocortex is responsible for higher cognitive functions and is essential for human consciousness.

The pulvinar sign seen on radiological imaging can indicate several possible conditions, including Alper’s Syndrome, cat-scratch disease, and post-infectious encephalitis. It may also be present in cases of M/V2 subtype of sporadic CJD, thalamic infarctions, and top-of-the-basilar ischemia. However, when considering vCJD, the pulvinar sign should be evaluated in the appropriate clinical context.

Creutzfeldt-Jakob Disease: Differences between vCJD and CJD

Creutzfeldt-Jakob Disease (CJD) is a prion disease that includes scrapie, BSE, and Kuru. However, there are important differences between sporadic (also known as classic) CJD and variant CJD. The table below summarizes these differences.

vCJD:
– Longer duration from onset of symptoms to death (a year of more)
– Presents with psychiatric and behavioral symptoms before neurological symptoms
– MRI shows pulvinar sign
– EEG shows generalized slowing
– Originates from infected meat products
– Affects younger people (age 25-30)

CJD:
– Shorter duration from onset of symptoms to death (a few months)
– Presents with neurological symptoms
– MRI shows bilateral anterior basal ganglia high signal
– EEG shows biphasic and triphasic waves 1-2 per second
– Originates from genetic mutation (bad luck)
– Affects older people (age 55-65)

Overall, understanding the differences between vCJD and CJD is important for diagnosis and treatment.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Norepinephrine: Synthesis, Release, and Breakdown

Norepinephrine is synthesized from tyrosine through a series of enzymatic reactions. The first step involves the conversion of tyrosine to L-DOPA by tyrosine hydroxylase. L-DOPA is then converted to dopamine by DOPA decarboxylase. Dopamine is further converted to norepinephrine by dopamine beta-hydroxylase. Finally, norepinephrine is converted to epinephrine by phenylethanolamine-N-methyltransferase.

The primary site of norepinephrine release is the locus coeruleus, also known as the blue spot, which is located in the pons. Once released, norepinephrine is broken down by two enzymes: catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). These enzymes play a crucial role in regulating the levels of norepinephrine in the body.

Broca’s aphasia is also known as non-fluent aphasia, while Wernicke’s aphasia is referred to as fluent aphasia.

Broca’s and Wernicke’s are two types of expressive dysphasia, which is characterized by difficulty producing speech despite intact comprehension. Dysarthria is a type of expressive dysphasia caused by damage to the speech production apparatus, while Broca’s aphasia is caused by damage to the area of the brain responsible for speech production, specifically Broca’s area located in Brodmann areas 44 and 45. On the other hand, Wernicke’s aphasia is a type of receptive of fluent aphasia caused by damage to the comprehension of speech, while the actual production of speech remains normal. Wernicke’s area is located in the posterior part of the superior temporal gyrus in the dominant hemisphere, within Brodmann area 22.

This question is presented in two variations on the exam, with one implying that auras are primarily linked to temporal lobe epilepsy and the other to complex partial seizures. In reality, partial seizures are most commonly associated with auras compared to other types of seizures. While partial seizures can originate in any lobe of the brain, those that arise in the temporal lobe are most likely to produce an aura. Therefore, both versions of the question are accurate.

Epilepsy and Aura

An aura is a subjective sensation that is a type of simple partial seizure. It typically lasts only a few seconds and can help identify the site of cortical onset. There are eight recognized types of auras, including somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic.

In about 80% of cases, auras precede temporal lobe seizures. The most common auras in these seizures are abdominal and psychic, which can cause a rising epigastric sensation of feelings of fear, déjà vu, of jamais vu. Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type, such as an electrical sensation of tingling. Occipital lobe seizures may begin with contralateral visual changes, such as colored lines, spots, of shapes, of even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.

Complex partial seizures are defined by impairment of consciousness, which means decreased responsiveness and awareness of oneself and surroundings. During a complex partial seizure, a patient is unresponsive and does not remember events that occurred.

Association fibres refer to axons that link different cortical areas within the same hemisphere of the brain. The middle longitudinal fasciculus is a white matter tract that connects the inferior parietal lobule to the temporal cortices. The uncinate fasciculus is a relatively short pathway that connects the anterior temporal areas to the inferior frontal areas. The inferior longitudinal fasciculus and inferior fronto-occipital fasciculus fibre pathways are believed to connect the occipital cortices to the anterior temporal and inferior frontal cortices (note that the inferior fronto-occipital fasciculus pathway is also known as the inferior occipitofrontal fasciculus). The cingulum is a group of white matter fibres that extend from the cingulate gyrus to the entorhinal cortex, facilitating communication between different parts of the limbic system.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Creutzfeldt-Jakob Disease: Differences between vCJD and CJD

Creutzfeldt-Jakob Disease (CJD) is a prion disease that includes scrapie, BSE, and Kuru. However, there are important differences between sporadic (also known as classic) CJD and variant CJD. The table below summarizes these differences.

vCJD:
– Longer duration from onset of symptoms to death (a year of more)
– Presents with psychiatric and behavioral symptoms before neurological symptoms
– MRI shows pulvinar sign
– EEG shows generalized slowing
– Originates from infected meat products
– Affects younger people (age 25-30)

CJD:
– Shorter duration from onset of symptoms to death (a few months)
– Presents with neurological symptoms
– MRI shows bilateral anterior basal ganglia high signal
– EEG shows biphasic and triphasic waves 1-2 per second
– Originates from genetic mutation (bad luck)
– Affects older people (age 55-65)

Overall, understanding the differences between vCJD and CJD is important for diagnosis and treatment.

Cranial Nerve Reflexes

When it comes to questions on cranial nerve reflexes, it is important to match the reflex to the nerves involved. Here are some examples:

– Pupillary light reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Accommodation reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Jaw jerk: involves the trigeminal nerve (sensory and motor).
– Corneal reflex: involves the trigeminal nerve (sensory) and facial nerve (motor).
– Vestibulo-ocular reflex: involves the vestibulocochlear nerve (sensory) and oculomotor, trochlear, and abducent nerves (motor).

Another example of a cranial nerve reflex is the gag reflex, which involves the glossopharyngeal nerve (sensory) and the vagus nerve (motor). This reflex is important for protecting the airway from foreign objects of substances that may trigger a gag reflex. It is also used as a diagnostic tool to assess the function of these nerves.

Sigma waves are typically observed during stage 2 sleep and are considered a normal occurrence during sleep. They usually follow muscle twitches and are believed to help maintain a peaceful state during sleep. These waves are produced in the reticular nucleus of the thalamus and arise from the interplay between the thalamus and the cortex. However, in familial fatal insomnia (a prion disease), the absence of sigma waves is a characteristic feature.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Cerebrospinal Fluid: Formation, Circulation, and Composition

Cerebrospinal fluid (CSF) is produced by ependymal cells in the choroid plexus of the lateral, third, and fourth ventricles. It is constantly reabsorbed, so only a small amount is present at any given time. CSF occupies the space between the arachnoid and pia mater and passes through various foramina and aqueducts to reach the subarachnoid space and spinal cord. It is then reabsorbed by the arachnoid villi and enters the dural venous sinuses.

The normal intracerebral pressure (ICP) is 5 to 15 mmHg, and the rate of formation of CSF is constant. The composition of CSF is similar to that of brain extracellular fluid (ECF) but different from plasma. CSF has a higher pCO2, lower pH, lower protein content, lower glucose concentration, higher chloride and magnesium concentration, and very low cholesterol content. The concentration of calcium and potassium is lower, while the concentration of sodium is unchanged.

CSF fulfills the role of returning interstitial fluid and protein to the circulation since there are no lymphatic channels in the brain. The blood-brain barrier separates CSF from blood, and only lipid-soluble substances can easily cross this barrier, maintaining the compositional differences.

Motor neuron Disease: A Progressive Neurodegenerative Condition

Motor neuron Disease (MND) is a condition that progressively damages the upper and lower motor neurons. This damage leads to muscle weakness and wasting, resulting in a loss of mobility in the limbs, as well as difficulties with speech, swallowing, and breathing. MND can be classified into four main types, including Amyotrophic lateral sclerosis, Progressive bulbar palsy, Progressive muscular atrophy, and Primary lateral sclerosis.

Macroscopic pathological features of MND include atrophy of the precentral gyrus and frontotemporal regions, thinning of the spinal cord, and atrophic anterior nerve roots. Microscopic changes involve the loss of motor neurons from the ventral horn of the spinal cord and lower brainstem. MND is a devastating condition that currently has no cure, and treatment is focused on managing symptoms and improving quality of life for those affected.

Understanding Action Potentials in Neurons and Muscle Cells

The membrane potential is a crucial aspect of cell physiology, and it exists across the plasma membrane of most cells. However, in neurons and muscle cells, this membrane potential can change over time. When a cell is not stimulated, it is in a resting state, and the inside of the cell is negatively charged compared to the outside. This resting membrane potential is typically around -70mV, and it is maintained by the Na/K pump, which maintains a high concentration of Na outside and K inside the cell.

To trigger an action potential, the membrane potential must be raised to around -55mV. This can occur when a neurotransmitter binds to the postsynaptic neuron and opens some ion channels. Once the membrane potential reaches -55mV, a cascade of events is initiated, leading to the opening of a large number of Na channels and causing the cell to depolarize. As the membrane potential reaches around +40 mV, the Na channels close, and the K gates open, allowing K to flood out of the cell and causing the membrane potential to fall back down. This process is irreversible and is critical for the transmission of signals in neurons and the contraction of muscle cells.

The Basal Ganglia: Functions and Disorders

The basal ganglia are a group of subcortical structures that play a crucial role in controlling movement and some cognitive processes. The components of the basal ganglia include the striatum (caudate, putamen, nucleus accumbens), subthalamic nucleus, globus pallidus, and substantia nigra (divided into pars compacta and pars reticulata). The putamen and globus pallidus are collectively referred to as the lenticular nucleus.

The basal ganglia are connected in a complex loop, with the cortex projecting to the striatum, the striatum to the internal segment of the globus pallidus, the internal segment of the globus pallidus to the thalamus, and the thalamus back to the cortex. This loop is responsible for regulating movement and cognitive processes.

However, problems with the basal ganglia can lead to several conditions. Huntington’s chorea is caused by degeneration of the caudate nucleus, while Wilson’s disease is characterized by copper deposition in the basal ganglia. Parkinson’s disease is associated with degeneration of the substantia nigra, and hemiballism results from damage to the subthalamic nucleus.

In summary, the basal ganglia are a crucial part of the brain that regulate movement and some cognitive processes. Disorders of the basal ganglia can lead to significant neurological conditions that affect movement and other functions.

Fatal familial insomnia (FFI) is characterized by minimal spongiform change, but notable thalamic atrophy and astrogliosis. Diagnosis of FFI relies heavily on immunohistochemistry and genotyping. In contrast, spongiform change is a hallmark of CJD and Kuru. The majority of CJD cases (85%) are sporadic, while only a small percentage are caused by consuming contaminated food (variant CJD of vCJD).

Lewy body dementia is a neurodegenerative disorder that is characterized by both macroscopic and microscopic changes in the brain. Macroscopically, there is cerebral atrophy, but it is less marked than in Alzheimer’s disease, and the brain weight is usually in the normal range. There is also pallor of the substantia nigra and the locus coeruleus, which are regions of the brain that produce dopamine and norepinephrine, respectively.

Microscopically, Lewy body dementia is characterized by the presence of intracellular protein accumulations called Lewy bodies. The major component of a Lewy body is alpha synuclein, and as they grow, they start to draw in other proteins such as ubiquitin. Lewy bodies are also found in Alzheimer’s disease, but they tend to be in the amygdala. They can also be found in healthy individuals, although it has been suggested that these may be pre-clinical cases of dementia with Lewy bodies. Lewy bodies are also found in other neurodegenerative disorders such as progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy.

In Lewy body dementia, Lewy bodies are mainly found within the brainstem, but they are also found in non-brainstem regions such as the amygdaloid nucleus, parahippocampal gyrus, cingulate cortex, and cerebral neocortex. Classic brainstem Lewy bodies are spherical intraneuronal cytoplasmic inclusions, characterized by hyaline eosinophilic cores, concentric lamellar bands, narrow pale halos, and immunoreactivity for alpha synuclein and ubiquitin. In contrast, cortical Lewy bodies typically lack a halo.

Most brains with Lewy body dementia also show some plaques and tangles, although in most instances, the lesions are not nearly as severe as in Alzheimer’s disease. Neuronal loss and gliosis are usually restricted to brainstem regions, particularly the substantia nigra and locus ceruleus.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Catecholamines are a group of chemical compounds that have a distinct structure consisting of a benzene ring with two hydroxyl groups, an intermediate ethyl chain, and a terminal amine group. These compounds play an important role in the body and are involved in various physiological processes. The three main catecholamines found in the body are dopamine, adrenaline, and noradrenaline. All of these compounds are derived from the amino acid tyrosine. Overall, catecholamines are essential for maintaining proper bodily functions and are involved in a wide range of physiological processes.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Neuroimaging techniques can be divided into structural and functional types, although this distinction is becoming less clear as new techniques emerge. Structural techniques include computed tomography (CT) and magnetic resonance imaging (MRI), which use x-rays and magnetic fields, respectively, to produce images of the brain’s structure. Functional techniques, on the other hand, measure brain activity by detecting changes in blood flow of oxygen consumption. These include functional MRI (fMRI), emission tomography (PET and SPECT), perfusion MRI (pMRI), and magnetic resonance spectroscopy (MRS). Some techniques, such as diffusion tensor imaging (DTI), combine both structural and functional information to provide a more complete picture of the brain’s anatomy and function. DTI, for example, uses MRI to estimate the paths that water takes as it diffuses through white matter, allowing researchers to visualize white matter tracts.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

Parkinson’s Disease Pathology

Parkinson’s disease is a neurodegenerative disorder that affects the central nervous system. The pathology of Parkinson’s disease is very similar to that of Lewy body dementia. The macroscopic features of Parkinson’s disease include pallor of the substantia nigra (midbrain) and locus coeruleus (pons). The microscopic changes include the presence of Lewy bodies, which are intracellular aggregates of alpha-synuclein. Additionally, there is a loss of dopaminergic cells from the substantia nigra pars compacta. These changes contribute to the motor symptoms of Parkinson’s disease, such as tremors, rigidity, and bradykinesia. Understanding the pathology of Parkinson’s disease is crucial for developing effective treatments and improving the quality of life for those affected by this condition.

The ethmoid bone contains the cribriform plate, which acts as a barrier between the nasal cavity and the brain.

Cranial Fossae and Foramina

The cranium is divided into three regions known as fossae, each housing different cranial lobes. The anterior cranial fossa contains the frontal lobes and includes the frontal and ethmoid bones, as well as the lesser wing of the sphenoid. The middle cranial fossa contains the temporal lobes and includes the greater wing of the sphenoid, sella turcica, and most of the temporal bones. The posterior cranial fossa contains the occipital lobes, cerebellum, and medulla and includes the occipital bone.

There are several foramina in the skull that allow for the passage of various structures. The most important foramina likely to appear in exams are listed below:

– Foramen spinosum: located in the middle fossa and allows for the passage of the middle meningeal artery.
– Foramen ovale: located in the middle fossa and allows for the passage of the mandibular division of the trigeminal nerve.
– Foramen lacerum: located in the middle fossa and allows for the passage of the small meningeal branches of the ascending pharyngeal artery and emissary veins from the cavernous sinus.
– Foramen magnum: located in the posterior fossa and allows for the passage of the spinal cord.
– Jugular foramen: located in the posterior fossa and allows for the passage of cranial nerves IX, X, and XI.

Understanding the location and function of these foramina is essential for medical professionals, as they play a crucial role in the diagnosis and treatment of various neurological conditions.

Pathology Findings in Psychiatry

There are several pathology findings that are associated with various psychiatric conditions. Papp-Lantos bodies, for example, are visible in the CNS and are associated with multisystem atrophy. Pick bodies, on the other hand, are large, dark-staining aggregates of proteins in neurological tissue and are associated with frontotemporal dementia.

Lewy bodies are another common pathology finding in psychiatry and are associated with Parkinson’s disease and Lewy Body dementia. These are round, concentrically laminated, pale eosinophilic cytoplasmic inclusions that are aggregates of alpha-synuclein.

Other pathology findings include asteroid bodies, which are associated with sarcoidosis and berylliosis, and are acidophilic, stellate inclusions in giant cells. Barr bodies are associated with stains of X chromosomes and are inactivated X chromosomes that appear as a dark staining mass in contact with the nuclear membrane.

Mallory bodies are another common pathology finding and are associated with alcoholic hepatitis, alcoholic cirrhosis, Wilson’s disease, and primary-biliary cirrhosis. These are eosinophilic intracytoplasmic inclusions in hepatocytes that are made up of intermediate filaments, predominantly prekeratin.

Other pathology findings include Schaumann bodies, which are associated with sarcoidosis and berylliosis, and are concentrically laminated inclusions in giant cells. Zebra bodies are associated with Niemann-Pick disease, Tay-Sachs disease, of any of the mucopolysaccharidoses and are palisaded lamellated membranous cytoplasmic bodies seen in macrophages.

LE bodies, also known as hematoxylin bodies, are associated with SLE (lupus) and are nuclei of damaged cells with bound anti-nuclear antibodies that become homogeneous and loose chromatin pattern. Verocay bodies are associated with Schwannoma (Neurilemoma) and are palisades of nuclei at the end of a fibrillar bundle.

Hirano bodies are associated with normal aging but are more numerous in Alzheimer’s disease. These are eosinophilic, football-shaped inclusions seen in neurons of the brain. Neurofibrillary tangles are another common pathology finding in Alzheimer’s disease and are made up of microtubule-associated proteins and neurofilaments.

Kayser-Fleischer rings are associated with Wilson’s disease and are rings of discoloration on the cornea. Finally, Kuru plaques are associated with Kuru and Gerstmann-Sträussler syndrome and are sometimes present in patients with Creutzfeldt-Jakob disease (CJD). These are composed partly of a host-encoded prion protein.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

Functions of the Hypothalamus

The hypothalamus is a vital part of the brain that plays a crucial role in regulating various bodily functions. It receives and integrates sensory information about the internal environment and directs actions to control internal homeostasis. The hypothalamus contains several nuclei and fiber tracts, each with specific functions.

The suprachiasmatic nucleus (SCN) is responsible for regulating circadian rhythms. Neurons in the SCN have an intrinsic rhythm of discharge activity and receive input from the retina. The SCN is considered the body’s master clock, but it has multiple connections with other hypothalamic nuclei.

Body temperature control is mainly under the control of the preoptic, anterior, and posterior nuclei, which have temperature-sensitive neurons. As the temperature goes above 37ºC, warm-sensitive neurons are activated, triggering parasympathetic activity to promote heat loss. As the temperature goes below 37ºC, cold-sensitive neurons are activated, triggering sympathetic activity to promote conservation of heat.

The hypothalamus also plays a role in regulating prolactin secretion. Dopamine is tonically secreted by dopaminergic neurons that project from the arcuate nucleus of the hypothalamus into the anterior pituitary gland via the tuberoinfundibular pathway. The dopamine that is released acts on lactotrophic cells through D2-receptors, inhibiting prolactin synthesis. In the absence of pregnancy of lactation, prolactin is constitutively inhibited by dopamine. Dopamine antagonists result in hyperprolactinemia, while dopamine agonists inhibit prolactin secretion.

In summary, the hypothalamus is a complex structure that regulates various bodily functions, including circadian rhythms, body temperature, and prolactin secretion. Dysfunction of the hypothalamus can lead to various disorders, such as sleep-rhythm disorder, diabetes insipidus, hyperprolactinemia, and obesity.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

The retina and optic nerves originate from protrusions of the diencephalon known as eye vesicles during development.

Neurodevelopment: Understanding Brain Development

The development of the central nervous system begins with the neuroectoderm, a specialized region of ectoderm. The embryonic brain is divided into three areas: the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon further divides into the telencephalon and diencephalon, while the hindbrain subdivides into the metencephalon and myelencephalon.

The telencephalon, of cerebrum, consists of the cerebral cortex, underlying white matter, and the basal ganglia. The diencephalon includes the prethalamus, thalamus, hypothalamus, subthalamus, epithalamus, and pretectum. The mesencephalon comprises the tectum, tegmentum, ventricular mesocoelia, cerebral peduncles, and several nuclei and fasciculi.

The rhombencephalon includes the medulla, pons, and cerebellum, which can be subdivided into a variable number of transversal swellings called rhombomeres. In humans, eight rhombomeres can be distinguished, from caudal to rostral: Rh7-Rh1 and the isthmus. Rhombomeres Rh7-Rh4 form the myelencephalon, while Rh3-Rh1 form the metencephalon.

Understanding neurodevelopment is crucial in comprehending brain development and its complexities. By studying the different areas of the embryonic brain, we can gain insight into the formation of the central nervous system and its functions.

Kluver-Bucy Syndrome: Causes and Symptoms

Kluver-Bucy syndrome is a neurological disorder that results from bilateral medial temporal lobe dysfunction, particularly in the amygdala. This condition is characterized by a range of symptoms, including hyperorality (a tendency to explore objects with the mouth), hypersexuality, docility, visual agnosia, and dietary changes.

The most common causes of Kluver-Bucy syndrome include herpes, late-stage Alzheimer’s disease, frontotemporal dementia, trauma, and bilateral temporal lobe infarction. In some cases, the condition may be reversible with treatment, but in others, it may be permanent and require ongoing management. If you of someone you know is experiencing symptoms of Kluver-Bucy syndrome, it is important to seek medical attention promptly to determine the underlying cause and develop an appropriate treatment plan.

Frontotemporal lobe degeneration (FTLD) encompasses various syndromes, such as Pick’s disease, primary progressive aphasia (which impacts speech), semantic dementia (affecting conceptual knowledge), and corticobasal degeneration (characterized by asymmetrical akinetic-rigid syndrome and apraxia). It is important to note that posterior cortical atrophy, which involves tissue loss in the posterior regions and affects higher visual processing, is not considered a part of the FTLD syndrome.