Understanding the Autonomic Nervous System

The autonomic nervous system is responsible for regulating involuntary functions in the body, such as heart rate, digestion, and sexual arousal. It is composed of two main components, the sympathetic and parasympathetic nervous systems, as well as a sensory division. The sympathetic division arises from the T1-L2/3 region of the spinal cord and synapses onto postganglionic neurons at paravertebral or prevertebral ganglia. The parasympathetic division arises from cranial nerves and the sacral spinal cord and synapses with postganglionic neurons at parasympathetic ganglia. The sensory division includes baroreceptors and chemoreceptors that monitor blood levels of oxygen, carbon dioxide, and glucose, as well as arterial pressure and the contents of the stomach and intestines.

The autonomic nervous system releases neurotransmitters such as noradrenaline and acetylcholine to achieve necessary functions and regulate homeostasis. The sympathetic nervous system causes fight or flight responses, while the parasympathetic nervous system causes rest and digest responses. Autonomic dysfunction refers to the abnormal functioning of any part of the autonomic nervous system, which can present in many forms and affect any of the autonomic systems. To assess a patient for autonomic dysfunction, a detailed history should be taken, and the patient should undergo a full neurological examination and further testing if necessary. Understanding the autonomic nervous system is crucial in diagnosing and treating autonomic dysfunction.

When the musculocutaneous nerve is injured, it can result in weakness when flexing the upper arm at the shoulder and elbow. This nerve is responsible for innervating the brachialis, biceps brachii, and coracobrachialis muscles. Other nerves, such as the axillary nerve, median nerve, and radial nerve, also play a role in muscle innervation and movement. The axillary nerve innervates the teres minor and deltoid muscles, while the median nerve innervates the majority of the flexor muscles in the forearm, the thenar muscles, and the two lateral lumbricals. The radial nerve innervates the triceps brachii and the muscles in the posterior compartment of the forearm, which generally cause extension of the wrist and fingers.

The Musculocutaneous Nerve: Function and Pathway

The musculocutaneous nerve is a nerve branch that originates from the lateral cord of the brachial plexus. Its pathway involves penetrating the coracobrachialis muscle and passing obliquely between the biceps brachii and the brachialis to the lateral side of the arm. Above the elbow, it pierces the deep fascia lateral to the tendon of the biceps brachii and continues into the forearm as the lateral cutaneous nerve of the forearm.

The musculocutaneous nerve innervates the coracobrachialis, biceps brachii, and brachialis muscles. Injury to this nerve can cause weakness in flexion at the shoulder and elbow. Understanding the function and pathway of the musculocutaneous nerve is important in diagnosing and treating injuries or conditions that affect this nerve.

The uvula deviating away from the side of the lesion indicates a problem with the left vagus nerve, as this nerve controls the muscles of the soft palate and can cause uvula deviation when damaged. In cases of vagus nerve lesions, the uvula deviates in the opposite direction of the lesion. As the patient’s uvula deviates towards the right, the underlying issue must be with the left vagus nerve.

The left hypoglossal nerve cannot be the cause of the uvula deviation, as this nerve only provides motor innervation to the tongue muscles and cannot affect the uvula.

Similarly, the right hypoglossal nerve and right trigeminal nerve cannot cause uvula deviation, as they do not have any control over the uvula. Trigeminal nerve lesions may cause different clinical signs depending on the location of the lesion, such as masseteric wasting in the case of mandibular nerve damage.

Cranial nerves are a set of 12 nerves that emerge from the brain and control various functions of the head and neck. Each nerve has a specific function, such as smell, sight, eye movement, facial sensation, and tongue movement. Some nerves are sensory, some are motor, and some are both. A useful mnemonic to remember the order of the nerves is Some Say Marry Money But My Brother Says Big Brains Matter Most, with S representing sensory, M representing motor, and B representing both.

In addition to their specific functions, cranial nerves also play a role in various reflexes. These reflexes involve an afferent limb, which carries sensory information to the brain, and an efferent limb, which carries motor information from the brain to the muscles. Examples of cranial nerve reflexes include the corneal reflex, jaw jerk, gag reflex, carotid sinus reflex, pupillary light reflex, and lacrimation reflex. Understanding the functions and reflexes of the cranial nerves is important in diagnosing and treating neurological disorders.

Anticipation may be observed in Huntington’s disease due to its nature as a trinucleotide repeat disorder. The disease is caused by an autosomal dominant gene with CAG repeats in exon 1 of the Huntingtin gene. The number of CAG repeats is indicative of the severity of the disease, with individuals having 36 to 39 repeats potentially developing symptoms, while those with 40 or more repeats almost always develop the disorder. HD can occur in individuals with 36 to 120 CAG repeats.

Anticipation is observed as the number of CAG repeats increases between generations. Offspring of individuals with 27 to 35 CAG repeats are at risk of developing HD, even though the parent does not suffer from the disease. Additionally, higher numbers of CAG repeats tend to cause HD to manifest at earlier ages, resulting in younger generations being affected by the disease.

Huntington’s disease is a genetic disorder that causes progressive and incurable neurodegeneration. It is inherited in an autosomal dominant manner and is caused by a trinucleotide repeat expansion of CAG in the huntingtin gene on chromosome 4. This can result in the phenomenon of anticipation, where the disease presents at an earlier age in successive generations. The disease leads to the degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia, which can cause a range of symptoms.

Typically, symptoms of Huntington’s disease develop after the age of 35 and can include chorea, personality changes such as irritability, apathy, and depression, intellectual impairment, dystonia, and saccadic eye movements. Unfortunately, there is currently no cure for Huntington’s disease, and it usually results in death around 20 years after the initial symptoms develop.

The most common cause of meningitis in adults is Streptococcus pneumoniae, which is also the likely pathogen in this patient’s case. His symptoms and lumbar puncture results suggest bacterial meningitis, with turbid fluid, raised opening pressure, and low glucose. While Escherichia coli is a common cause of meningitis in infants under 3 months, it is less likely in a 29-year-old. Haemophilus influenzae B is also an unlikely cause in this patient, who is up-to-date with their vaccinations and beyond the age range for this pathogen. Staphylococcus pneumoniae is a rare but serious cause of pneumonia, but not as likely as Streptococcus pneumoniae to be the cause of this patient’s symptoms.

Aetiology of Meningitis in Adults

Meningitis is a condition that can be caused by various infectious agents such as bacteria, viruses, and fungi. However, this article will focus on bacterial meningitis. The most common bacteria that cause meningitis in adults is Streptococcus pneumoniae, which can develop after an episode of otitis media. Another bacterium that can cause meningitis is Neisseria meningitidis. Listeria monocytogenes is more common in immunocompromised patients and the elderly. Lastly, Haemophilus influenzae type b is also a known cause of meningitis in adults. It is important to identify the causative agent of meningitis to provide appropriate treatment and prevent complications.

The arachnoid villi are responsible for absorbing cerebrospinal fluid into the venous sinuses of the brain. On the other hand, the choroid plexus produces and releases cerebrospinal fluid. The inferior colliculus is involved in the auditory pathway, while the corpus callosum allows communication between the left and right hemispheres of the brain. The pia mater is the innermost layer of the meninges and is impermeable to fluid. Normal pressure hydrocephalus is a condition that presents with gait abnormality, urinary incontinence, and dementia, and is characterized by dilation of the ventricular system on imaging.

Cerebrospinal Fluid: Circulation and Composition

Cerebrospinal fluid (CSF) is a clear, colorless liquid that fills the space between the arachnoid mater and pia mater, covering the surface of the brain. The total volume of CSF in the brain is approximately 150ml, and it is produced by the ependymal cells in the choroid plexus or blood vessels. The majority of CSF is produced by the choroid plexus, accounting for 70% of the total volume. The remaining 30% is produced by blood vessels. The CSF is reabsorbed via the arachnoid granulations, which project into the venous sinuses.

The circulation of CSF starts from the lateral ventricles, which are connected to the third ventricle via the foramen of Munro. From the third ventricle, the CSF flows through the cerebral aqueduct (aqueduct of Sylvius) to reach the fourth ventricle via the foramina of Magendie and Luschka. The CSF then enters the subarachnoid space, where it circulates around the brain and spinal cord. Finally, the CSF is reabsorbed into the venous system via arachnoid granulations into the superior sagittal sinus.

The composition of CSF is essential for its proper functioning. The glucose level in CSF is between 50-80 mg/dl, while the protein level is between 15-40 mg/dl. Red blood cells are not present in CSF, and the white blood cell count is usually less than 3 cells/mm3. Understanding the circulation and composition of CSF is crucial for diagnosing and treating various neurological disorders.

The choroid plexus is a branching structure resembling sea coral that contains specialized ependymal cells responsible for producing and releasing cerebrospinal fluid (CSF). It is present in all four ventricles of the brain, with the largest portion located in the lateral ventricles. The choroid plexus plays a role in removing waste products from the CSF.

The inferior colliculus is a nucleus in the midbrain involved in the auditory pathway. There are two inferior colliculi, one on each side of the midbrain, and they are part of the corpora quadrigemina along with the two superior colliculi (involved in the visual pathway).

Arachnoid villi are microscopic projections of the arachnoid membrane that allow for the absorption of cerebrospinal fluid into the venous system. This is important as the amount of CSF produced each day is four times the total volume of the ventricular system.

The corpus callosum is a bundle of nerve fibers that connects the left and right hemispheres of the brain, allowing for communication between them.

The pineal gland is a small protrusion on the brain that produces melatonin and regulates the sleep cycle.

A sudden-onset severe headache, described as the worst ever experienced, may indicate a subarachnoid hemorrhage. This can occur with or without trauma and is characterized by a thunderclap headache. If a CT scan is normal, CSF should be examined for xanthochromia, which is a yellow coloration that occurs several hours after a subarachnoid hemorrhage due to the breakdown of red blood cells and the release of bilirubin into the CSF.

Cerebrospinal Fluid: Circulation and Composition

Cerebrospinal fluid (CSF) is a clear, colorless liquid that fills the space between the arachnoid mater and pia mater, covering the surface of the brain. The total volume of CSF in the brain is approximately 150ml, and it is produced by the ependymal cells in the choroid plexus or blood vessels. The majority of CSF is produced by the choroid plexus, accounting for 70% of the total volume. The remaining 30% is produced by blood vessels. The CSF is reabsorbed via the arachnoid granulations, which project into the venous sinuses.

The circulation of CSF starts from the lateral ventricles, which are connected to the third ventricle via the foramen of Munro. From the third ventricle, the CSF flows through the cerebral aqueduct (aqueduct of Sylvius) to reach the fourth ventricle via the foramina of Magendie and Luschka. The CSF then enters the subarachnoid space, where it circulates around the brain and spinal cord. Finally, the CSF is reabsorbed into the venous system via arachnoid granulations into the superior sagittal sinus.

The composition of CSF is essential for its proper functioning. The glucose level in CSF is between 50-80 mg/dl, while the protein level is between 15-40 mg/dl. Red blood cells are not present in CSF, and the white blood cell count is usually less than 3 cells/mm3. Understanding the circulation and composition of CSF is crucial for diagnosing and treating various neurological disorders.

Footdrop, which is impaired dorsiflexion of the ankle, can be caused by a lesion of the common peroneal nerve. This nerve is a branch of the sciatic nerve and divides into the deep and superficial peroneal nerves after wrapping around the neck of the fibula. The deep peroneal nerve is responsible for innervating muscles that control dorsiflexion of the foot, such as the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. Damage to the common or deep peroneal nerve can result in weakness or paralysis of these muscles, leading to unopposed plantar flexion of the foot. The superficial peroneal nerve, on the other hand, innervates muscles that evert the foot. Other nerves that innervate muscles in the lower limb include the femoral nerve, which controls hip flexion and knee extension, the tibial nerve, which mainly controls plantar flexion and inversion of the foot, and the obturator nerve, which mainly controls thigh adduction.

The common peroneal nerve originates from the dorsal divisions of the sacral plexus, specifically from L4, L5, S1, and S2. This nerve provides sensation to the skin and fascia of the anterolateral surface of the leg and dorsum of the foot, as well as innervating the muscles of the anterior and peroneal compartments of the leg, extensor digitorum brevis, and the knee, ankle, and foot joints. It is located laterally within the sciatic nerve and passes through the lateral and proximal part of the popliteal fossa, under the cover of biceps femoris and its tendon, to reach the posterior aspect of the fibular head. The common peroneal nerve divides into the deep and superficial peroneal nerves at the point where it winds around the lateral surface of the neck of the fibula in the body of peroneus longus, approximately 2 cm distal to the apex of the head of the fibula. It is palpable posterior to the head of the fibula. The nerve has several branches, including the nerve to the short head of biceps, articular branch (knee), lateral cutaneous nerve of the calf, and superficial and deep peroneal nerves at the neck of the fibula.

The sphenoid bone contains the foramen spinosum, through which the middle meningeal artery and vein pass.

Foramina of the Base of the Skull

The base of the skull contains several openings called foramina, which allow for the passage of nerves, blood vessels, and other structures. The foramen ovale, located in the sphenoid bone, contains the mandibular nerve, otic ganglion, accessory meningeal artery, and emissary veins. The foramen spinosum, also in the sphenoid bone, contains the middle meningeal artery and meningeal branch of the mandibular nerve. The foramen rotundum, also in the sphenoid bone, contains the maxillary nerve.

The foramen lacerum, located in the sphenoid bone, is initially occluded by a cartilaginous plug and contains the internal carotid artery, nerve and artery of the pterygoid canal, and the base of the medial pterygoid plate. The jugular foramen, located in the temporal bone, contains the inferior petrosal sinus, glossopharyngeal, vagus, and accessory nerves, sigmoid sinus, and meningeal branches from the occipital and ascending pharyngeal arteries.

The foramen magnum, located in the occipital bone, contains the anterior and posterior spinal arteries, vertebral arteries, and medulla oblongata. The stylomastoid foramen, located in the temporal bone, contains the stylomastoid artery and facial nerve. Finally, the superior orbital fissure, located in the sphenoid bone, contains the oculomotor nerve, recurrent meningeal artery, trochlear nerve, lacrimal, frontal, and nasociliary branches of the ophthalmic nerve, and abducent nerve.

The jugular foramen serves as the pathway for the glossopharyngeal nerve. This nerve has autonomic functions for the parotid gland, motor functions for the stylopharyngeus muscle, and sensory functions for the posterior third of the tongue, palatine tonsils, oropharynx, middle ear mucosa, pharyngeal tympanic tube, and carotid bodies.

Cranial nerves are a set of 12 nerves that emerge from the brain and control various functions of the head and neck. Each nerve has a specific function, such as smell, sight, eye movement, facial sensation, and tongue movement. Some nerves are sensory, some are motor, and some are both. A useful mnemonic to remember the order of the nerves is Some Say Marry Money But My Brother Says Big Brains Matter Most, with S representing sensory, M representing motor, and B representing both.

In addition to their specific functions, cranial nerves also play a role in various reflexes. These reflexes involve an afferent limb, which carries sensory information to the brain, and an efferent limb, which carries motor information from the brain to the muscles. Examples of cranial nerve reflexes include the corneal reflex, jaw jerk, gag reflex, carotid sinus reflex, pupillary light reflex, and lacrimation reflex. Understanding the functions and reflexes of the cranial nerves is important in diagnosing and treating neurological disorders.

When a hemisection of the spinal cord occurs, it results in a condition known as Brown-Sequard syndrome. This condition is characterized by sensory and motor loss on the same side of the injury, as well as pain loss on the opposite side. The loss of motor function on the same side is due to damage to the corticospinal tract, which does not cross over within the spinal cord but instead decussates in the brainstem. Similarly, the loss of light touch on the same side is due to damage to the dorsal column, which also decussates in the brainstem. In contrast, the loss of pain on the opposite side is due to damage to the spinothalamic tract, which decussates at the level of sensory input. As a result, pain signals are always carried on the opposite side of the spinal cord, while motor and light touch signals are carried on the same side as the injury.

Understanding Brown-Sequard Syndrome

Brown-Sequard syndrome is a condition that occurs when there is a lateral hemisection of the spinal cord. This condition is characterized by a combination of symptoms that affect the body’s ability to sense and move. Individuals with Brown-Sequard syndrome experience weakness on the same side of the body as the lesion, as well as a loss of proprioception and vibration sensation on that side. On the opposite side of the body, there is a loss of pain and temperature sensation.

It is important to note that the severity of Brown-Sequard syndrome can vary depending on the location and extent of the spinal cord injury. Some individuals may experience only mild symptoms, while others may have more severe impairments. Treatment for Brown-Sequard syndrome typically involves a combination of physical therapy, medication, and other supportive measures to help manage symptoms and improve overall quality of life.

The recovery from syncopal episodes is rapid and the postictal period is short. In contrast, seizures have a much longer postictal period. The stem suggests that the syncope may be due to exam stress and poor nutrition habits. One way to differentiate between seizures and syncope is by the length of the postictal period, with syncope having a quick recovery. Lip smacking is not associated with syncope, but rather with focal seizures of the temporal lobe. The 10-minute postictal period described in the stem is not consistent with a seizure.

Epilepsy is a neurological condition that causes recurrent seizures. In the UK, around 500,000 people have epilepsy, and two-thirds of them can control their seizures with antiepileptic medication. While epilepsy usually occurs in isolation, certain conditions like cerebral palsy, tuberous sclerosis, and mitochondrial diseases have an association with epilepsy. It’s important to note that seizures can also occur due to other reasons like infection, trauma, or metabolic disturbance.

Seizures can be classified into focal seizures, which start in a specific area of the brain, and generalised seizures, which involve networks on both sides of the brain. Patients who have had generalised seizures may experience biting their tongue or incontinence of urine. Following a seizure, patients typically have a postictal phase where they feel drowsy and tired for around 15 minutes.

Patients who have had their first seizure generally undergo an electroencephalogram (EEG) and neuroimaging (usually a MRI). Most neurologists start antiepileptics following a second epileptic seizure. Antiepileptics are one of the few drugs where it is recommended that we prescribe by brand, rather than generically, due to the risk of slightly different bioavailability resulting in a lowered seizure threshold.

Patients who drive, take other medications, wish to get pregnant, or take contraception need to consider the possible interactions of the antiepileptic medication. Some commonly used antiepileptics include sodium valproate, carbamazepine, lamotrigine, and phenytoin. In case of a seizure that doesn’t terminate after 5-10 minutes, medication like benzodiazepines may be administered to terminate the seizure. If a patient continues to fit despite such measures, they are said to have status epilepticus, which is a medical emergency requiring hospital treatment.

The patient’s symptoms are consistent with acute closed-angle glaucoma, which is an urgent ophthalmological emergency. They are experiencing a headache with unilateral eye pain, reduced vision, visual haloes, a red and congested eye with a cloudy cornea, and a dilated, unresponsive pupil. These symptoms may be triggered by darkness or dilating eye drops. Treatment should involve laying the patient flat to relieve angle pressure, administering pilocarpine eye drops to constrict the pupil, acetazolamide orally to reduce aqueous humour production, and providing analgesia. Referral to secondary care is necessary.

It is important to differentiate this condition from other potential causes of the patient’s symptoms. Central retinal vein occlusion, for example, would cause sudden painless loss of vision and severe retinal haemorrhages on fundoscopy. Migraines typically involve a visual or somatosensory aura followed by a unilateral throbbing headache, nausea, vomiting, and photophobia. Subarachnoid haemorrhages present with a sudden, severe headache, rather than a gradually worsening one accompanied by eye signs. Temporal arteritis may cause pain when chewing, difficulty brushing hair, and thickened temporal arteries visible on examination. However, the presence of a dilated, fixed pupil with conjunctival injection should steer the clinician away from a diagnosis of migraine.

Acute angle closure glaucoma (AACG) is a type of glaucoma where there is a rise in intraocular pressure (IOP) due to a blockage in the outflow of aqueous humor. This condition is more likely to occur in individuals with hypermetropia, pupillary dilation, and lens growth associated with aging. Symptoms of AACG include severe pain, decreased visual acuity, a hard and red eye, haloes around lights, and a semi-dilated non-reacting pupil. AACG is an emergency and requires urgent referral to an ophthalmologist. The initial medical treatment involves a combination of eye drops, such as a direct parasympathomimetic, a beta-blocker, and an alpha-2 agonist, as well as intravenous acetazolamide to reduce aqueous secretions. Definitive management involves laser peripheral iridotomy, which creates a tiny hole in the peripheral iris to allow aqueous humor to flow to the angle.

Dementia comes in various forms, with Alzheimer’s dementia (AD) being the most prevalent. AD is characterized by a gradual onset that is difficult to pinpoint, and there are no other indications of any other cause. Vascular Dementia, on the other hand, has a sudden onset and progresses in a stepwise manner. Patients may remain stable for a while before suddenly progressing to the next level, resulting in a fluctuating course. They also have uneven impairment and neurological signs, and typically have vascular risk factors such as cardiovascular disease or peripheral vascular disease. Lewy body dementia is characterized by fluctuating levels of consciousness, visual hallucinations, parkinsonian-like symptoms, falls, and neuroleptic sensitivity.

Vascular dementia is a group of syndromes of cognitive impairment caused by different mechanisms resulting from cerebrovascular disease. It is the second most common form of dementia after Alzheimer’s disease and accounts for around 17% of dementia in the UK. The main subtypes of VD are stroke-related VD, subcortical VD, and mixed dementia. Risk factors include a history of stroke or TIA, atrial fibrillation, hypertension, diabetes mellitus, hyperlipidaemia, smoking, obesity, and coronary heart disease. Diagnosis is made based on a comprehensive history and physical examination, formal screen for cognitive impairment, and MRI scan. Treatment is mainly symptomatic, and non-pharmacological management includes tailored cognitive stimulation programs, multisensory stimulation, music and art therapy, and animal-assisted therapy. There is no specific pharmacological treatment approved for cognitive symptoms, and AChE inhibitors or memantine should only be considered for people with suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia, or dementia with Lewy bodies.

In Alzheimer’s disease, the pathology involves extraneuronal amyloid plaques and intraneuronal neurofibrillary tangles. Amyloid plaques are clumps of beta-amyloid that are found in the extracellular matrix, while neurofibrillary tangles are made up of hyperphosphorylated tau and are located within the neurons. The exact role of beta-amyloid and tau in the development of Alzheimer’s disease is still not fully understood.

Alzheimer’s disease is a type of dementia that gradually worsens over time and is caused by the degeneration of the brain. There are several risk factors associated with Alzheimer’s disease, including increasing age, family history, and certain genetic mutations. The disease is also more common in individuals of Caucasian ethnicity and those with Down’s syndrome.

The pathological changes associated with Alzheimer’s disease include widespread cerebral atrophy, particularly in the cortex and hippocampus. Microscopically, there are cortical plaques caused by the deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein. The hyperphosphorylation of the tau protein has been linked to Alzheimer’s disease. Additionally, there is a deficit of acetylcholine due to damage to an ascending forebrain projection.

Neurofibrillary tangles are a hallmark of Alzheimer’s disease and are partly made from a protein called tau. Tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules. In Alzheimer’s disease, tau proteins are excessively phosphorylated, impairing their function.

Brachial Plexus Injuries: Erb-Duchenne and Klumpke’s Paralysis

Erb-Duchenne paralysis is a type of brachial plexus injury that results from damage to the C5 and C6 roots. This can occur during a breech presentation, where the baby’s head and neck are pulled to the side during delivery. Symptoms of Erb-Duchenne paralysis include weakness or paralysis of the arm, shoulder, and hand, as well as a winged scapula.

On the other hand, Klumpke’s paralysis is caused by damage to the T1 root of the brachial plexus. This type of injury typically occurs due to traction, such as when a baby’s arm is pulled during delivery. Klumpke’s paralysis can result in a loss of intrinsic hand muscles, which can affect fine motor skills and grip strength.

It is important to note that brachial plexus injuries can have long-term effects on a person’s mobility and quality of life. Treatment options may include physical therapy, surgery, or a combination of both. Early intervention is key to improving outcomes and minimizing the impact of these injuries.

Hemisensory loss in this patient, along with a history of hypertension, is highly indicative of a lacunar infarct. Lacunar strokes are closely linked to hypertension.

Facial pain on the same side and pain in the limbs and torso on the opposite side are typical symptoms of lateral medullary syndrome.

Contralateral homonymous hemianopia is a common symptom of middle cerebral artery strokes.

Lateral pontine syndrome is characterized by deafness on the same side as the lesion.

Stroke can affect different parts of the brain depending on which artery is affected. If the anterior cerebral artery is affected, the person may experience weakness and loss of sensation on the opposite side of the body, with the lower extremities being more affected than the upper. If the middle cerebral artery is affected, the person may experience weakness and loss of sensation on the opposite side of the body, with the upper extremities being more affected than the lower. They may also experience vision loss and difficulty with language. If the posterior cerebral artery is affected, the person may experience vision loss and difficulty recognizing objects.

Lacunar strokes are a type of stroke that are strongly associated with hypertension. They typically present with isolated weakness or loss of sensation on one side of the body, or weakness with difficulty coordinating movements. They often occur in the basal ganglia, thalamus, or internal capsule.

This individual is experiencing Broca’s dysphasia, which is characterized by non-fluent speech, normal comprehension, and impaired repetition. This is likely due to a recent neurological insult that has resulted in higher cognitive dysfunction, specifically aphasia. Broca’s area, located in the posterior inferior frontal gyrus of the dominant hemisphere, is responsible for generating compressible words and is typically supplied by the superior division of the left MCA. Conductive aphasia, on the other hand, involves normal, fluent speech but poor repetition and is caused by a stroke involving the connection between different areas of the brain.

Types of Aphasia: Understanding the Different Forms of Language Impairment

Aphasia is a language disorder that affects a person’s ability to communicate effectively. There are different types of aphasia, each with its own set of symptoms and underlying causes. Wernicke’s aphasia, also known as receptive aphasia, is caused by a lesion in the superior temporal gyrus. This area is responsible for forming speech before sending it to Broca’s area. People with Wernicke’s aphasia may speak fluently, but their sentences often make no sense, and they may use word substitutions and neologisms. Comprehension is impaired.

Broca’s aphasia, also known as expressive aphasia, is caused by a lesion in the inferior frontal gyrus. This area is responsible for speech production. People with Broca’s aphasia may speak in a non-fluent, labored, and halting manner. Repetition is impaired, but comprehension is normal.

Conduction aphasia is caused by a stroke affecting the arcuate fasciculus, the connection between Wernicke’s and Broca’s area. People with conduction aphasia may speak fluently, but their repetition is poor. They are aware of the errors they are making, but comprehension is normal.

Global aphasia is caused by a large lesion affecting all three areas mentioned above, resulting in severe expressive and receptive aphasia. People with global aphasia may still be able to communicate using gestures. Understanding the different types of aphasia is important for proper diagnosis and treatment.

The hypoglossal canal is the pathway for the hypoglossal nerve.

Foramina of the Base of the Skull

The base of the skull contains several openings called foramina, which allow for the passage of nerves, blood vessels, and other structures. The foramen ovale, located in the sphenoid bone, contains the mandibular nerve, otic ganglion, accessory meningeal artery, and emissary veins. The foramen spinosum, also in the sphenoid bone, contains the middle meningeal artery and meningeal branch of the mandibular nerve. The foramen rotundum, also in the sphenoid bone, contains the maxillary nerve.

The foramen lacerum, located in the sphenoid bone, is initially occluded by a cartilaginous plug and contains the internal carotid artery, nerve and artery of the pterygoid canal, and the base of the medial pterygoid plate. The jugular foramen, located in the temporal bone, contains the inferior petrosal sinus, glossopharyngeal, vagus, and accessory nerves, sigmoid sinus, and meningeal branches from the occipital and ascending pharyngeal arteries.

The foramen magnum, located in the occipital bone, contains the anterior and posterior spinal arteries, vertebral arteries, and medulla oblongata. The stylomastoid foramen, located in the temporal bone, contains the stylomastoid artery and facial nerve. Finally, the superior orbital fissure, located in the sphenoid bone, contains the oculomotor nerve, recurrent meningeal artery, trochlear nerve, lacrimal, frontal, and nasociliary branches of the ophthalmic nerve, and abducent nerve.

The posterior pituitary gland is formed by neural cells’ axons that extend directly from the hypothalamus.

In contrast to the anterior pituitary gland, which has separate hormone-secreting cells controlled by hormonal stimulation, the posterior pituitary gland only contains neural cells that extend from the hypothalamus. Therefore, the hormones (ADH and oxytocin) released from the posterior pituitary gland are released from the axons of cells extending from the hypothalamus.

All anterior pituitary hormone release is controlled through hormonal stimulation from the hypothalamus.

The adrenal medulla directly releases epinephrine, norepinephrine, and small amounts of dopamine from sympathetic neural cells.

The pituitary gland is a small gland located within the sella turcica in the sphenoid bone of the middle cranial fossa. It weighs approximately 0.5g and is covered by a dural fold. The gland is attached to the hypothalamus by the infundibulum and receives hormonal stimuli from the hypothalamus through the hypothalamo-pituitary portal system. The anterior pituitary, which develops from a depression in the wall of the pharynx known as Rathkes pouch, secretes hormones such as ACTH, TSH, FSH, LH, GH, and prolactin. GH and prolactin are secreted by acidophilic cells, while ACTH, TSH, FSH, and LH are secreted by basophilic cells. On the other hand, the posterior pituitary, which is derived from neuroectoderm, secretes ADH and oxytocin. Both hormones are produced in the hypothalamus before being transported by the hypothalamo-hypophyseal portal system.

Extrapyramidal symptoms such as akathisia, bradykinesia, dystonia, and tardive dyskinesia are commonly observed in Parkinsonian conditions. Babinski’s sign, which is the upward movement of the big toe upon stimulation of the sole of the foot, is normal in infants but may indicate upper motor neuron dysfunction in older individuals. The presence of these symptoms suggests a possible diagnosis of Parkinsonism, as discussed in the case.

Parkinsonism is a condition that can be caused by various factors. One of the most common causes is Parkinson’s disease, which is a degenerative disorder of the nervous system. Other causes include drug-induced Parkinsonism, which can occur as a side effect of certain medications such as antipsychotics and metoclopramide. Progressive supranuclear palsy, multiple system atrophy, Wilson’s disease, post-encephalitis, dementia pugilistica, and exposure to toxins such as carbon monoxide and MPTP can also lead to Parkinsonism.

It is important to note that not all medications that can cause Parkinsonism have the same effect. For example, domperidone does not cross the blood-brain barrier and therefore does not cause extrapyramidal side-effects. Parkinsonism can have a significant impact on a person’s quality of life, and it is important to identify the underlying cause in order to provide appropriate treatment and management. With proper care and management, individuals with Parkinsonism can lead fulfilling lives.

Timolol, a beta blocker, is an effective treatment for primary open-angle glaucoma as it reduces the production of aqueous humor in the eye. This condition is caused by a gradual increase in intraocular pressure due to poor drainage within the trabecular meshwork, resulting in gradual vision loss. The first-line treatments for primary open-angle glaucoma include beta blockers, prostaglandin analogues, carbonic anhydrase inhibitors, and alpha-2-agonists. However, if a patient is unable to tolerate carbonic anhydrase inhibitors, prostaglandin analogues, or alpha-2-agonists, beta blockers like timolol are the remaining option. Carbonic anhydrase inhibitors reduce aqueous humor production, prostaglandin analogues increase uveoscleral outflow, and alpha-2-agonists have a dual action of reducing humor production and increasing outflow. It is important to note that increasing aqueous humor production and reducing uveoscleral outflow are not effective treatments for glaucoma.

Primary open-angle glaucoma is a type of optic neuropathy that is associated with increased intraocular pressure (IOP). It is classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye. In open-angle glaucoma, the iris is clear of the meshwork, but the trabecular network offers increased resistance to aqueous outflow, causing increased IOP. This condition affects 0.5% of people over the age of 40 and its prevalence increases with age up to 10% over the age of 80 years. Both males and females are equally affected. The main causes of primary open-angle glaucoma are increasing age and genetics, with first-degree relatives of an open-angle glaucoma patient having a 16% chance of developing the disease.

Primary open-angle glaucoma is characterised by a slow rise in intraocular pressure, which is symptomless for a long period. It is typically detected following an ocular pressure measurement during a routine examination by an optometrist. Signs of the condition include increased intraocular pressure, visual field defect, and pathological cupping of the optic disc. Case finding and provisional diagnosis are done by an optometrist, and referral to an ophthalmologist is done via the GP. Final diagnosis is made through investigations such as automated perimetry to assess visual field, slit lamp examination with pupil dilatation to assess optic nerve and fundus for a baseline, applanation tonometry to measure IOP, central corneal thickness measurement, and gonioscopy to assess peripheral anterior chamber configuration and depth. The risk of future visual impairment is assessed using risk factors such as IOP, central corneal thickness (CCT), family history, and life expectancy.

The majority of patients with primary open-angle glaucoma are managed with eye drops that aim to lower intraocular pressure and prevent progressive loss of visual field. According to NICE guidelines, the first line of treatment is a prostaglandin analogue (PGA) eyedrop, followed by a beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop as a second line of treatment. Surgery or laser treatment can be tried in more advanced cases. Reassessment is important to exclude progression and visual field loss and needs to be done more frequently if IOP is uncontrolled, the patient is high risk, or there

This region receives cutaneous sensation from the median nerve.

Anatomy and Function of the Median Nerve

The median nerve is a nerve that originates from the lateral and medial cords of the brachial plexus. It descends lateral to the brachial artery and passes deep to the bicipital aponeurosis and the median cubital vein at the elbow. The nerve then passes between the two heads of the pronator teres muscle and runs on the deep surface of flexor digitorum superficialis. Near the wrist, it becomes superficial between the tendons of flexor digitorum superficialis and flexor carpi radialis, passing deep to the flexor retinaculum to enter the palm.

The median nerve has several branches that supply the upper arm, forearm, and hand. These branches include the pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis, flexor pollicis longus, and palmar cutaneous branch. The nerve also provides motor supply to the lateral two lumbricals, opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis muscles, as well as sensory supply to the palmar aspect of the lateral 2 ½ fingers.

Damage to the median nerve can occur at the wrist or elbow, resulting in various symptoms such as paralysis and wasting of thenar eminence muscles, weakness of wrist flexion, and sensory loss to the palmar aspect of the fingers. Additionally, damage to the anterior interosseous nerve, a branch of the median nerve, can result in loss of pronation of the forearm and weakness of long flexors of the thumb and index finger. Understanding the anatomy and function of the median nerve is important in diagnosing and treating conditions that affect this nerve.

The Spinothalamic Tract and its Function in Sensory Transmission

The spinothalamic tract is responsible for transmitting impulses from receptors that measure crude touch, pain, and temperature. It is composed of two tracts, the lateral and anterior spinothalamic tracts, with the former transmitting pain and temperature and the latter crude touch and pressure.

Before decussating in the spinal cord, neurons transmitting these signals ascend by one or two vertebral levels in Lissaurs tract. Once they have crossed over, they pass rostrally in the cord to connect at the thalamus. This pathway is crucial in the transmission of sensory information from the body to the brain, allowing us to perceive and respond to various stimuli.

Overall, the spinothalamic tract plays a vital role in our ability to sense and respond to our environment. Its function in transmitting sensory information is essential for our survival and well-being.

Wernicke’s aphasia is caused by damage to the superior temporal gyrus, resulting in fluent speech but poor comprehension and characteristic ‘word salad’. Patients with this type of aphasia are often unaware of their errors.

Conduction aphasia, on the other hand, is caused by damage to the arcuate fasciculus, which connects Wernicke’s and Broca’s areas. This results in fluent speech with poor repetition, but patients are usually aware of their errors.

A lesion of the corpus callosum can cause more widespread problems with motor and sensory deficits due to impaired communication between the hemispheres.

Broca’s area, located in the inferior frontal gyrus, is responsible for expressive aphasia, where speech is non-fluent but comprehension is intact.

It’s important to note that true aphasia does not involve any motor deficits, so damage to the primary motor cortex would not be the cause.

Types of Aphasia: Understanding the Different Forms of Language Impairment

Aphasia is a language disorder that affects a person’s ability to communicate effectively. There are different types of aphasia, each with its own set of symptoms and underlying causes. Wernicke’s aphasia, also known as receptive aphasia, is caused by a lesion in the superior temporal gyrus. This area is responsible for forming speech before sending it to Broca’s area. People with Wernicke’s aphasia may speak fluently, but their sentences often make no sense, and they may use word substitutions and neologisms. Comprehension is impaired.

Broca’s aphasia, also known as expressive aphasia, is caused by a lesion in the inferior frontal gyrus. This area is responsible for speech production. People with Broca’s aphasia may speak in a non-fluent, labored, and halting manner. Repetition is impaired, but comprehension is normal.

Conduction aphasia is caused by a stroke affecting the arcuate fasciculus, the connection between Wernicke’s and Broca’s area. People with conduction aphasia may speak fluently, but their repetition is poor. They are aware of the errors they are making, but comprehension is normal.

Global aphasia is caused by a large lesion affecting all three areas mentioned above, resulting in severe expressive and receptive aphasia. People with global aphasia may still be able to communicate using gestures. Understanding the different types of aphasia is important for proper diagnosis and treatment.

Unilateral damage to the cerebellum results in symptoms that are on the same side as the lesion. In this case, if the right cerebellum is damaged, the individual may experience dysdiadochokinesia, ataxia, nystagmus, intention tremor, scanning dysarthria, and a positive heel-shin test. Damage to the left cerebellum would not cause symptoms on the right side. Damage to the left temporal lobe may result in changes in behavior and emotions, forgetfulness, disruptions in the sense of smell, taste, and hearing, and language and speech disorders. Damage to the right parietal lobe may cause alexia, agraphia, acalculia, left-sided hemi-spatial neglect, homonymous inferior quadrantanopia, loss of sensations like touch, apraxias, or astereognosis.

Cerebellar syndrome is a condition that affects the cerebellum, a part of the brain responsible for coordinating movement and balance. When there is damage or injury to one side of the cerebellum, it can cause symptoms on the same side of the body. These symptoms can be remembered using the mnemonic DANISH, which stands for Dysdiadochokinesia, Dysmetria, Ataxia, Nystagmus, Intention tremour, Slurred staccato speech, and Hypotonia.

There are several possible causes of cerebellar syndrome, including genetic conditions like Friedreich’s ataxia and ataxic telangiectasia, neoplastic growths like cerebellar haemangioma, strokes, alcohol use, multiple sclerosis, hypothyroidism, and certain medications or toxins like phenytoin or lead poisoning. In some cases, cerebellar syndrome may be a paraneoplastic condition, meaning it is a secondary effect of an underlying cancer like lung cancer. It is important to identify the underlying cause of cerebellar syndrome in order to provide appropriate treatment and management.

Todd’s palsy, which is often linked to epilepsy, is a temporary paralysis that occurs after a seizure. It should not be confused with Bell’s palsy, which affects the facial nerve, or Erb’s palsy, which affects the nerves in the upper limb, particularly C5-6. Additionally, transient ischemic attacks (TIAs) and cerebellar tonsil herniation, which is caused by increased pressure within the skull, are not related to Todd’s palsy.

Epilepsy Classification: Understanding Seizures

Epilepsy is a neurological disorder that affects millions of people worldwide. The classification of epilepsy has undergone changes in recent years, with the new basic seizure classification based on three key features. The first feature is where seizures begin in the brain, followed by the level of awareness during a seizure, which is important as it can affect safety during a seizure. The third feature is other features of seizures.

Focal seizures, previously known as partial seizures, start in a specific area on one side of the brain. The level of awareness can vary in focal seizures, and they can be further classified as focal aware, focal impaired awareness, and awareness unknown. Focal seizures can also be classified as motor or non-motor, or having other features such as aura.

Generalized seizures involve networks on both sides of the brain at the onset, and consciousness is lost immediately. The level of awareness in the above classification is not needed, as all patients lose consciousness. Generalized seizures can be further subdivided into motor and non-motor, with specific types including tonic-clonic, tonic, clonic, typical absence, and atonic.

Unknown onset is a term reserved for when the origin of the seizure is unknown. Focal to bilateral seizure starts on one side of the brain in a specific area before spreading to both lobes, previously known as secondary generalized seizures. Understanding the classification of epilepsy and the different types of seizures can help in the diagnosis and management of this condition.

The index finger and thumb are the primary locations of the C6 dermatome.

Understanding Dermatomes: Major Landmarks and Mnemonics

Dermatomes are areas of skin that are innervated by a single spinal nerve. Understanding dermatomes is important in diagnosing and treating various neurological conditions. The major dermatome landmarks are listed in the table above, along with helpful mnemonics to aid in memorization.

Starting at the top of the body, the C2 dermatome covers the posterior half of the skull, resembling a cap. Moving down to C3, it covers the area of a high turtleneck shirt, while C4 covers the area of a low-collar shirt. The C5 dermatome runs along the ventral axial line of the upper limb, while C6 covers the thumb and index finger. To remember this, make a 6 with your left hand by touching the tip of your thumb and index finger together.

Moving down to the middle finger and palm of the hand, the C7 dermatome is located here, while the C8 dermatome covers the ring and little finger. The T4 dermatome is located at the nipples, while T5 covers the inframammary fold. The T6 dermatome is located at the xiphoid process, and T10 covers the umbilicus. To remember this, think of BellybuT-TEN.

The L1 dermatome covers the inguinal ligament, while L4 covers the knee caps. To remember this, think of being Down on aLL fours with the number 4 representing the knee caps. The L5 dermatome covers the big toe and dorsum of the foot (except the lateral aspect), while the S1 dermatome covers the lateral foot and small toe. To remember this, think of S1 as the smallest one. Finally, the S2 and S3 dermatomes cover the genitalia.

Understanding dermatomes and their landmarks can aid in diagnosing and treating various neurological conditions. The mnemonics provided can help in memorizing these important landmarks.

The bladder is under autonomic control from the hypogastric plexuses, while voluntary control of the urethral sphincter is provided by the pudendal nerve.

The Pudendal Nerve and its Functions

The pudendal nerve is a nerve that originates from the S2, S3, and S4 nerve roots and exits the pelvis through the greater sciatic foramen. It then re-enters the perineum through the lesser sciatic foramen. This nerve provides innervation to the anal sphincters and external urethral sphincter, as well as cutaneous innervation to the perineum surrounding the anus and posterior vulva.

Late onset pudendal neuropathy may occur due to traction and compression of the pudendal nerve by the foetus during late pregnancy. This condition may contribute to the development of faecal incontinence. Understanding the functions of the pudendal nerve is important in diagnosing and treating conditions related to the perineum and surrounding areas.

The hypothalamus is responsible for regulating body temperature, as it controls thermoregulation. It responds to pyrogens produced during infections, which induce the synthesis of prostaglandins that bind to receptors in the hypothalamus and raise body temperature. The cerebellum, limbic system, and pineal gland are not involved in temperature control.

The hypothalamus is a part of the brain that plays a crucial role in maintaining the body’s internal balance, or homeostasis. It is located in the diencephalon and is responsible for regulating various bodily functions. The hypothalamus is composed of several nuclei, each with its own specific function. The anterior nucleus, for example, is involved in cooling the body by stimulating the parasympathetic nervous system. The lateral nucleus, on the other hand, is responsible for stimulating appetite, while lesions in this area can lead to anorexia. The posterior nucleus is involved in heating the body and stimulating the sympathetic nervous system, and damage to this area can result in poikilothermia. Other nuclei include the septal nucleus, which regulates sexual desire, the suprachiasmatic nucleus, which regulates circadian rhythm, and the ventromedial nucleus, which is responsible for satiety. Lesions in the paraventricular nucleus can lead to diabetes insipidus, while lesions in the dorsomedial nucleus can result in savage behavior.