GABA-A is the sole ionotropic receptor among the options provided. Its function involves the selective conduction of chloride ions across the cell membrane upon activation by GABA, leading to hyperpolarization of the neuron.

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.

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.

The pituitary gland is situated in the sella turcica, while the suprachiasmatic nucleus regulates circadian rhythms. Serotonin release in the brain is primarily sourced from the neurons of the raphe nuclei, which are located along the midline of the brainstem. The choroid plexus produces cerebrospinal fluid, and enterochromaffin cells in the gut contain the majority of the body’s serotonin.

Simultagnosia is a condition where an individual is unable to focus on more than one aspect of a complex scene at a time. This condition, along with optic ataxia and oculomotor apraxia, is part of Balint’s syndrome.

Gerstmann syndrome is characterized by four symptoms: dysgraphia/agraphia, dyscalculia/acalculia, finger agnosia, and left-right disorientation. This syndrome is linked to a lesion in the dominant parietal lobe, specifically the left side of the angular and supramarginal gyri. It is rare for an individual to present with all four symptoms of the tetrad.

Dementia pugilistica, also known as CTE, is categorized as a tauopathy, which is a type of neurodegenerative disease that involves the accumulation of tau protein into NFTs of gliofibrillary tangles in the brain. While it commonly occurs due to repeated brain injuries, it can also develop from a single traumatic event, as reported by Smith in 2013.

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.

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 Edinger-Westphal nucleus is the motor nucleus of the third cranial nerve, while the putamen and globus pallidus comprise the lenticular nucleus, which is part of the basal ganglia. The basal ganglia play a role in motor control and use the inhibitory neurotransmitter GABA. The components of the basal ganglia can be classified in various ways, with the corpus striatum (caudate nucleus, putamen, nucleus accumbens, and globus pallidus) and the striatum of neostriatum (caudate, putamen, and globus pallidus) being common groupings.

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.

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.

Actin is the primary component of Hirano bodies, which are indicative of neurodegeneration but lack specificity.

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.

Glutamate is the primary neurotransmitter responsible for excitatory signaling in the brain.

Glutamate: The Most Abundant Neurotransmitter in the Brain

Glutamate is a neurotransmitter that is found in abundance in the brain. It is always excitatory and can act through both ionotropic and metabotropic receptors. This neurotransmitter is believed to play a crucial role in learning and memory processes. Its ability to stimulate neurons and enhance synaptic plasticity is thought to be responsible for its role in memory formation. Glutamate is also involved in various other brain functions, including motor control, sensory perception, and emotional regulation. Its importance in the brain makes it a target for various neurological disorders, including Alzheimer’s disease, Parkinson’s disease, and epilepsy.

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.

The BOLD technique is used by fMRI to non-invasively map cortical activation, while PET and SPECT require the administration of a radioactive isotope and are invasive. Although all three magnetic imaging techniques are non-invasive, fMRI stands out for its use of the BOLD technique.

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.

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).

HPA Axis Dysfunction in Mood Disorders

The HPA axis, which includes regulatory neural inputs and a feedback loop involving the hypothalamus, pituitary, and adrenal glands, plays a central role in the stress response. Excessive secretion of cortisol, a glucocorticoid hormone, can lead to disruptions in cellular functioning and widespread physiologic dysfunction. Dysregulation of the HPA axis is implicated in mood disorders such as depression and bipolar affective disorder.

In depressed patients, cortisol levels often do not decrease as expected in response to the administration of dexamethasone, a synthetic corticosteroid. This abnormality in the dexamethasone suppression test is thought to be linked to genetic of acquired defects of glucocorticoid receptors. Tricyclic antidepressants have been shown to increase expression of glucocorticoid receptors, whereas this is not the case for SSRIs.

Early adverse experiences can produce long standing changes in HPA axis regulation, indicating a possible neurobiological mechanism whereby childhood trauma could be translated into increased vulnerability to mood disorder. In major depression, there is hypersecretion of cortisol, corticotropin-releasing factor (CRF), and ACTH, and associated adrenocortical enlargement. HPA abnormalities have also been found in other psychiatric disorders including Alzheimer’s and PTSD.

In bipolar disorder, dysregulation of ACTH and cortisol response after CRH stimulation have been reported. Abnormal DST results are found more often during depressive episodes in the course of bipolar disorder than in unipolar disorder. Reduced pituitary volume secondary to LHPA stimulation, resulting in pituitary hypoactivity, has been observed in bipolar patients.

Overall, HPA axis dysfunction is implicated in mood disorders, and understanding the underlying mechanisms may lead to new opportunities for treatments.

Dura Mater

The dura mater is one of the three membranes, known as meninges, that cover the brain and spinal cord. It is the outermost and most fibrous layer, with the pia mater and arachnoid mater making up the remaining layers. The pia mater is the innermost layer.

The dura mater is folded at certain points, including the falx cerebri, which separates the two cerebral hemispheres of the brain, the tentorium cerebelli, which separates the cerebellum from the cerebrum, the falx cerebelli, which separates the cerebellar hemispheres, and the sellar diaphragm, which covers the pituitary gland and forms a roof over the hypophyseal fossa.

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.

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.

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.

Understanding Prosopagnosia: The Inability to Recognize Faces

Prosopagnosia, also known as face blindness, is a condition where individuals are unable to recognize faces. This complex process involves various areas of the brain, with the fusiform gyrus in the temporal lobe being the most significant. The inability to recognize faces can be caused by damage to this area of the brain of can be a result of a developmental disorder.

The condition can be challenging for individuals as it can affect their ability to recognize familiar faces, including family members and friends. It can also impact their social interactions and make it difficult to navigate social situations. While there is no cure for prosopagnosia, individuals can learn to use other cues such as voice, clothing, and context to recognize people.

Understanding prosopagnosia is crucial in providing support and accommodations for individuals who experience this condition. It is essential to raise awareness and promote research to develop effective interventions to help individuals with face blindness.

Anton’s syndrome, also known as Anton-Babinski syndrome, is a condition that results from damage to the occipital lobe. People with this syndrome are cortically blind, but they are not aware of it and deny having any problem, a condition known as anosognosia. They may start falling over furniture as they cannot see, but they believe they can still see and describe their surroundings in detail, even though their descriptions are incorrect (confabulation). This syndrome is characterized by a lack of awareness of visual impairment, which can lead to significant difficulties in daily life.

Brain Structures and Functions

The brain is a complex organ that is responsible for controlling various bodily functions. Among the important structures in the brain are the substantia nigra, hippocampus, hypothalamus, pituitary gland, and thalamus.

The substantia nigra is a part of the basal ganglia located in the midbrain. It contains dopamine-producing neurons that regulate voluntary movement and mood. Parkinson’s disease is associated with the degeneration of the melanin-containing cells in the pars compacta of the substantia nigra.

The hippocampus is a part of the limbic system that is involved in memory, learning, attention, and information processing.

The hypothalamus is located at the base of the brain near the pituitary gland. It regulates thirst, hunger, circadian rhythm, emotions, and body temperature. It also controls the pituitary gland by secreting hormones.

The pituitary gland is a small endocrine organ located below the hypothalamus in the middle of the base of the brain. It controls many bodily functions through the action of hormones and is divided into an anterior lobe, intermediate lobe, and posterior lobe.

The thalamus is located above the brainstem and processes and relays sensory and motor information.

If the individual were to experience impaired consciousness during the attack, this would be classified as a complex partial seizure. However, based on the current symptoms, it appears to be a simple partial seizure with retained consciousness.

Hemiballismus is an uncommon condition that arises following a stroke affecting the basal ganglia, particularly the subthalamic nucleus. It is typically identified by uncontrolled flinging movements of the limbs, which can be forceful and have a broad range of motion. These movements are unpredictable and ongoing, and may affect either the proximal or distal muscles on one side of the body.

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.

The Papez Circuit: A Neural Pathway for Emotion

James Papez was the first to describe a neural pathway in the brain that mediates the process of emotion. This pathway is known as the ‘Papez circuit’ and is located on the medial surface of the brain. It is bilateral, symmetrical, and links the cortex to the hypothalamus.

According to Papez, information about emotion passes through several structures in the brain, including the hippocampus, the Mammillary bodies of the hypothalamus, the anterior nucleus of the thalamus, the cingulate cortex, and the entorhinal cortex. Finally, the information passes through the hippocampus again, completing the circuit.

The Papez circuit was one of the first descriptions of the limbic system, which is responsible for regulating emotions, motivation, and memory. Understanding the Papez circuit and the limbic system has important implications for understanding and treating emotional disorders such as anxiety and depression.

Indicators of a potentially serious headache are:

– Developing a headache for the first time after the age of 50
– Sudden and severe headache (often described as a thunderclap headache)
– Accompanying symptoms such as redness in the eye and seeing halos around lights
– Headache that gets worse with physical activity of straining (such as during a Valsalva maneuver)

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.

Deep brain stimulation (DBS) for treatment resistant depression targets specific brain regions based on their known involvement in pleasure, reward, and mood regulation. The nucleus accumbens is targeted due to its role in pleasure and reward processing. The inferior thalamic peduncle is targeted based on PET studies showing hyperactivity in depression. The lateral habenula is chosen due to observed hypermetabolism in depressed patients. The subgenual cingulate gyrus is targeted due to its hyperactivity in depression. The ventral capsule/ventral striatum is chosen based on its association with improved mood and reduced depressive symptoms following ablation treatments for OCD and depression.

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.

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.