The triangular space serves as a pathway for the radial nerve to exit the axilla. Its upper boundary is defined by the teres major muscle, which has a close association with the radial nerve.

The Radial Nerve: Anatomy, Innervation, and Patterns of Damage

The radial nerve is a continuation of the posterior cord of the brachial plexus, with root values ranging from C5 to T1. It travels through the axilla, posterior to the axillary artery, and enters the arm between the brachial artery and the long head of triceps. From there, it spirals around the posterior surface of the humerus in the groove for the radial nerve before piercing the intermuscular septum and descending in front of the lateral epicondyle. At the lateral epicondyle, it divides into a superficial and deep terminal branch, with the deep branch crossing the supinator to become the posterior interosseous nerve.

The radial nerve innervates several muscles, including triceps, anconeus, brachioradialis, and extensor carpi radialis. The posterior interosseous branch innervates supinator, extensor carpi ulnaris, extensor digitorum, and other muscles. Denervation of these muscles can lead to weakness or paralysis, with effects ranging from minor effects on shoulder stability to loss of elbow extension and weakening of supination of prone hand and elbow flexion in mid prone position.

Damage to the radial nerve can result in wrist drop and sensory loss to a small area between the dorsal aspect of the 1st and 2nd metacarpals. Axillary damage can also cause paralysis of triceps. Understanding the anatomy, innervation, and patterns of damage of the radial nerve is important for diagnosing and treating conditions that affect this nerve.

The abducens nerve, also known as CN VI, is vulnerable to increased pressure within the skull due to its lengthy path within the cranial cavity. Additionally, it travels over the petrous temporal bone, making it susceptible to sixth nerve palsies that can occur in cases of mastoiditis.

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.

Foot drop is a possible consequence of sciatic nerve damage. The patient in question may have a herniated disc caused by heavy lifting, which is compressing their sciatic nerve and leading to weakness in the foot dorsiflexors.

If a person experiences pain when they abduct their hip, it could be due to damage to the superior gluteal nerve.

Damage to the femoral nerve can cause pain when extending the knee, as well as pain when flexing the thigh.

Femoral nerve damage can also result in loss of sensation over the medial aspect of the thigh, as well as the anterior aspect of the thigh and lower leg.

Damage to the lateral cutaneous nerve of the thigh can cause loss of sensation over the posterior surface of the thigh, as well as the lateral surface of the thigh.

Understanding Foot Drop: Causes and Examination

Foot drop is a condition that occurs when the foot dorsiflexors become weak. This can be caused by various factors, including a common peroneal nerve lesion, L5 radiculopathy, sciatic nerve lesion, superficial or deep peroneal nerve lesion, or central nerve lesions. However, the most common cause is a common peroneal nerve lesion, which is often due to compression at the neck of the fibula. This can be triggered by certain positions, prolonged confinement, recent weight loss, Baker’s cysts, or plaster casts to the lower leg.

To diagnose foot drop, a thorough examination is necessary. If the patient has an isolated peroneal neuropathy, there will be weakness of foot dorsiflexion and eversion, and reflexes will be normal. Weakness of hip abduction is suggestive of an L5 radiculopathy. Bilateral symptoms, fasciculations, or other abnormal neurological findings are indications for specialist referral.

If foot drop is diagnosed, conservative management is appropriate. Patients should avoid leg crossing, squatting, and kneeling. Symptoms typically improve over 2-3 months.

The two end branches of the lateral cord of the brachial plexus are the lateral root of the median nerve and the musculocutaneous nerve. If the musculocutaneous nerve is damaged, it can result in weakened elbow flexion. The posterior cord has two end branches, the axillary nerve and radial nerve. The lateral pectoral nerve is a branch of the lateral cord but not an end branch. The medial cord has two end branches, the medial root of the median nerve and the ulnar nerve.

Brachial Plexus Cords and their Origins

The brachial plexus cords are categorized based on their position in relation to the axillary artery. These cords pass over the first rib near the lung’s dome and under the clavicle, just behind the subclavian artery. The lateral cord is formed by the anterior divisions of the upper and middle trunks and gives rise to the lateral pectoral nerve, which originates from C5, C6, and C7. The medial cord is formed by the anterior division of the lower trunk and gives rise to the medial pectoral nerve, the medial brachial cutaneous nerve, and the medial antebrachial cutaneous nerve, which originate from C8, T1, and C8, T1, respectively. The posterior cord is formed by the posterior divisions of the three trunks (C5-T1) and gives rise to the upper and lower subscapular nerves, the thoracodorsal nerve to the latissimus dorsi (also known as the middle subscapular nerve), and the axillary and radial nerves.

The deep brachial artery, also known as the profunda brachii artery, arises from the brachial artery just below the teres major muscle. It runs closely alongside the radial nerve in the radial groove and provides blood supply to structures in the posterior aspect of the forearm. The brachial artery divides into the radial and ulnar arteries at the cubital fossa. It is important to note that the profunda femoris vein and great saphenous vein are located in the leg, not the arm.

Anatomy of the Brachial Artery

The brachial artery is a continuation of the axillary artery and runs from the lower border of teres major to the cubital fossa where it divides into the radial and ulnar arteries. It is located in the upper arm and has various relations with surrounding structures. Posteriorly, it is related to the long head of triceps with the radial nerve and profunda vessels in between. Anteriorly, it is overlapped by the medial border of biceps. The median nerve crosses the artery in the middle of the arm. In the cubital fossa, the brachial artery is separated from the median cubital vein by the bicipital aponeurosis. The basilic vein is in contact with the most proximal aspect of the cubital fossa and lies medially. Understanding the anatomy of the brachial artery is important for medical professionals when performing procedures such as blood pressure measurement or arterial line placement.

Mechanothermal stimuli are transmitted slowly through C fibres, while A α fibres transmit motor proprioception information, A β fibres transmit touch and pressure information, and B fibres are responsible for autonomic functions.

Neurons and Synaptic Signalling

Neurons are the building blocks of the nervous system and are made up of dendrites, a cell body, and axons. They can be classified by their anatomical structure, axon width, and function. Neurons communicate with each other at synapses, which consist of a presynaptic membrane, synaptic gap, and postsynaptic membrane. Neurotransmitters are small chemical messengers that diffuse across the synaptic gap and activate receptors on the postsynaptic membrane. Different neurotransmitters have different effects, with some causing excitation and others causing inhibition. The deactivation of neurotransmitters varies, with some being degraded by enzymes and others being reuptaken by cells. Understanding the mechanisms of neuronal communication is crucial for understanding the functioning of the nervous system.

The patient is likely experiencing an inferior homonymous quadrantanopia due to a lesion in the superior optic radiations of the parietal lobe. This type of visual field defect occurs when there is damage to the opposite side of the brain from where the defect is present. Lesions in the inferior temporal lobe result in superior defects, while lesions in the superior parietal lobe result in inferior defects. It is important to note that the left superior optic radiations are located in the parietal lobe, not the temporal lobe, and therefore a lesion in the left superior optic radiations in the temporal lobe is not possible. Additionally, a lesion in the right inferior optic radiations in the parietal lobe or the right superior optic radiations in the temporal lobe would not cause a defect on the patient’s right side, as the lesion must be on the opposite side of the brain from the defect.

Understanding Visual Field Defects

Visual field defects can occur due to various reasons, including lesions in the optic tract, optic radiation, or occipital cortex. A left homonymous hemianopia indicates a visual field defect to the left, which is caused by a lesion in the right optic tract. On the other hand, homonymous quadrantanopias can be categorized into PITS (Parietal-Inferior, Temporal-Superior) and can be caused by lesions in the inferior or superior optic radiations in the temporal or parietal lobes.

When it comes to congruous and incongruous defects, the former refers to complete or symmetrical visual field loss, while the latter indicates incomplete or asymmetric visual field loss. Incongruous defects are caused by optic tract lesions, while congruous defects are caused by optic radiation or occipital cortex lesions. In cases where there is macula sparing, it is indicative of a lesion in the occipital cortex.

Bitemporal hemianopia, on the other hand, is caused by a lesion in the optic chiasm. The type of defect can indicate the location of the compression, with an upper quadrant defect being more common in inferior chiasmal compression, such as a pituitary tumor, and a lower quadrant defect being more common in superior chiasmal compression, such as a craniopharyngioma.

Understanding visual field defects is crucial in diagnosing and treating various neurological conditions. By identifying the type and location of the defect, healthcare professionals can provide appropriate interventions to improve the patient’s quality of life.

Temporal lobe seizures can be identified by the presence of lip smacking and postictal dysphasia. These symptoms, along with a recurrent sense of déjà vu, suggest that the seizure is localized in the temporal lobe. Seizures in other parts of the brain, such as the frontal, occipital, or parietal lobes, typically present with different symptoms. Generalized seizures affecting the entire brain result in loss of consciousness and generalized tonic-clonic seizures.

Localising Features of Focal Seizures in Epilepsy

Focal seizures in epilepsy can be localised based on the specific location of the brain where they occur. Temporal lobe seizures are common and may occur with or without impairment of consciousness or awareness. Most patients experience an aura, which is typically a rising epigastric sensation, along with psychic or experiential phenomena such as déjà vu or jamais vu. Less commonly, hallucinations may occur, such as auditory, gustatory, or olfactory hallucinations. These seizures typically last around one minute and are often accompanied by automatisms, such as lip smacking, grabbing, or plucking.

On the other hand, frontal lobe seizures are characterised by motor symptoms such as head or leg movements, posturing, postictal weakness, and Jacksonian march. Parietal lobe seizures, on the other hand, are sensory in nature and may cause paraesthesia. Finally, occipital lobe seizures may cause visual symptoms such as floaters or flashes. By identifying the specific location and type of seizure, doctors can better diagnose and treat epilepsy in patients.

A right superior homonymous quadrantanopia in the patient is caused by a lesion in the left inferior optic radiation located in the temporal lobe. The sudden onset indicates a possible stroke or vascular event. A superior homonymous quadrantanopia occurs when the contralateral inferior optic radiation is affected.

A lesion in the left superior optic radiation would result in a right inferior homonymous quadrantanopia, which is not the case here. Similarly, a lesion in the left optic tract would cause contralateral hemianopia, which is also not the diagnosis in this patient.

Understanding Visual Field Defects

Visual field defects can occur due to various reasons, including lesions in the optic tract, optic radiation, or occipital cortex. A left homonymous hemianopia indicates a visual field defect to the left, which is caused by a lesion in the right optic tract. On the other hand, homonymous quadrantanopias can be categorized into PITS (Parietal-Inferior, Temporal-Superior) and can be caused by lesions in the inferior or superior optic radiations in the temporal or parietal lobes.

When it comes to congruous and incongruous defects, the former refers to complete or symmetrical visual field loss, while the latter indicates incomplete or asymmetric visual field loss. Incongruous defects are caused by optic tract lesions, while congruous defects are caused by optic radiation or occipital cortex lesions. In cases where there is macula sparing, it is indicative of a lesion in the occipital cortex.

Bitemporal hemianopia, on the other hand, is caused by a lesion in the optic chiasm. The type of defect can indicate the location of the compression, with an upper quadrant defect being more common in inferior chiasmal compression, such as a pituitary tumor, and a lower quadrant defect being more common in superior chiasmal compression, such as a craniopharyngioma.

Understanding visual field defects is crucial in diagnosing and treating various neurological conditions. By identifying the type and location of the defect, healthcare professionals can provide appropriate interventions to improve the patient’s quality of life.

The development of sensory and motor neurons is determined by the alar and basal plates, respectively.

Transcription factor expression in motor neurons is regulated by SHH signalling, which plays a crucial role in their development.

Hox genes are essential for the proper positioning of motor neurons along the cranio-caudal axis.

Motor neurons originate from the basal plates.

Interestingly, retinoic acid appears to facilitate the differentiation of motor neurons.

It is not possible for motor neurons to develop during week 4 of development, as the neural tube is still in the process of closing.

Embryonic Development of the Nervous System

The nervous system develops from the embryonic neural tube, which gives rise to the brain and spinal cord. The neural tube is divided into five regions, each of which gives rise to specific structures in the nervous system. The telencephalon gives rise to the cerebral cortex, lateral ventricles, and basal ganglia. The diencephalon gives rise to the thalamus, hypothalamus, optic nerves, and third ventricle. The mesencephalon gives rise to the midbrain and cerebral aqueduct. The metencephalon gives rise to the pons, cerebellum, and superior part of the fourth ventricle. The myelencephalon gives rise to the medulla and inferior part of the fourth ventricle.

The neural tube is also divided into two plates: the alar plate and the basal plate. The alar plate gives rise to sensory neurons, while the basal plate gives rise to motor neurons. This division of the neural tube into different regions and plates is crucial for the proper development and function of the nervous system. Understanding the embryonic development of the nervous system is important for understanding the origins of neurological disorders and for developing new treatments for these disorders.

A lower motor neuron lesion can be identified by a decrease in reflex response.

When a lower motor neuron lesion occurs, it can result in reduced tone, weakness, and muscle fasciculations. These neurons originate in the anterior horn of the spinal cord and connect with the neuromuscular junction.

On the other hand, if the corticospinal tract is affected in the motor cortex, internal capsule, midbrain, or medulla, it would cause an upper motor neuron pattern of weakness. This would be characterized by hypertonia, brisk reflexes, and an upgoing plantar reflex response.

Reflexes are automatic responses that our body makes in response to certain stimuli. These responses are controlled by the nervous system and do not require conscious thought. There are several common reflexes that are associated with specific roots in the spinal cord. For example, the ankle reflex is associated with the S1-S2 root, while the knee reflex is associated with the L3-L4 root. Similarly, the biceps reflex is associated with the C5-C6 root, and the triceps reflex is associated with the C7-C8 root. Understanding these reflexes can help healthcare professionals diagnose and treat certain conditions.

Understanding Chorioretinitis and Its Causes

Chorioretinitis is a medical condition that affects the retina and choroid, which are the two layers of tissue at the back of the eye. This condition is characterized by inflammation and damage to these tissues, which can lead to vision loss and other complications. There are several possible causes of chorioretinitis, including syphilis, cytomegalovirus, toxoplasmosis, sarcoidosis, and tuberculosis.

Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum. It can affect various parts of the body, including the eyes, and can lead to chorioretinitis if left untreated. Cytomegalovirus is a common virus that can cause chorioretinitis in people with weakened immune systems, such as those with HIV/AIDS. Toxoplasmosis is a parasitic infection that can be contracted from contaminated food or water, and can also cause chorioretinitis.

Sarcoidosis is a condition that causes inflammation in various parts of the body, including the eyes. It can lead to chorioretinitis as well as other eye problems such as uveitis and optic neuritis. Tuberculosis is a bacterial infection that can affect the lungs and other parts of the body, including the eyes. It can cause chorioretinitis as well as other eye problems such as iritis and scleritis.

In summary, chorioretinitis is a serious eye condition that can lead to vision loss and other complications. It can be caused by various infections and inflammatory conditions, including syphilis, cytomegalovirus, toxoplasmosis, sarcoidosis, and tuberculosis. Early diagnosis and treatment are essential for preventing further damage and preserving vision.

The mandibular nerve gives rise to several branches, including the auriculotemporal nerve, lingual nerve, inferior alveolar nerve, nerve to the mylohyoid, and mental nerve.

The facial nerve is responsible for supplying the muscles of facial expression, the digastric muscle, and various glandular structures. It also contains a few afferent fibers that originate in the genicular ganglion and are involved in taste. Bilateral facial nerve palsy can be caused by conditions such as sarcoidosis, Guillain-Barre syndrome, Lyme disease, and bilateral acoustic neuromas. Unilateral facial nerve palsy can be caused by these conditions as well as lower motor neuron issues like Bell’s palsy and upper motor neuron issues like stroke.

The upper motor neuron lesion typically spares the upper face, specifically the forehead, while a lower motor neuron lesion affects all facial muscles. The facial nerve’s path includes the subarachnoid path, where it originates in the pons and passes through the petrous temporal bone into the internal auditory meatus with the vestibulocochlear nerve. The facial canal path passes superior to the vestibule of the inner ear and contains the geniculate ganglion at the medial aspect of the middle ear. The stylomastoid foramen is where the nerve passes through the tympanic cavity anteriorly and the mastoid antrum posteriorly, and it also includes the posterior auricular nerve and branch to the posterior belly of the digastric and stylohyoid muscle.

During embryonic development, the metencephalon is responsible for the formation of the pons and cerebellum.

As the prosencephalon grows, it splits into two ear-shaped structures: the telencephalon (which develops into the hemispheres) and the diencephalon (which develops into the thalamus and hypothalamus).

The mesencephalon grows slowly, and its central cavity eventually becomes the cerebral aqueduct.

The rhombencephalon divides into two parts: the metencephalon (which forms the pons and cerebellum) and the myelencephalon (which forms the medulla).

Embryonic Development of the Nervous System

The nervous system develops from the embryonic neural tube, which gives rise to the brain and spinal cord. The neural tube is divided into five regions, each of which gives rise to specific structures in the nervous system. The telencephalon gives rise to the cerebral cortex, lateral ventricles, and basal ganglia. The diencephalon gives rise to the thalamus, hypothalamus, optic nerves, and third ventricle. The mesencephalon gives rise to the midbrain and cerebral aqueduct. The metencephalon gives rise to the pons, cerebellum, and superior part of the fourth ventricle. The myelencephalon gives rise to the medulla and inferior part of the fourth ventricle.

The neural tube is also divided into two plates: the alar plate and the basal plate. The alar plate gives rise to sensory neurons, while the basal plate gives rise to motor neurons. This division of the neural tube into different regions and plates is crucial for the proper development and function of the nervous system. Understanding the embryonic development of the nervous system is important for understanding the origins of neurological disorders and for developing new treatments for these disorders.

If Mark has a unilateral cerebellar lesion, he is likely to experience symptoms on the same side of his body as the lesion, which would be the left side in this case. The signs associated with cerebellar lesions include dysdiadochokinesia & dysmetria, ataxia, nystagmus, intention tremor, slurred speech, and hypotonia, and they would be more pronounced on the affected side of the body. As the lesion grows and affects both hemispheres, both sides of the body may become affected, but initially, left-sided symptoms are more likely. It is unlikely that Mark would develop right-sided symptoms, as this would be contralateral to the lesion. The location of the lesion within each hemisphere determines whether the upper or lower parts of the body are more affected.

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 ataxia 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.

Fluent speech may still be present despite neologisms and word substitution resulting from temporal lobe lesions. Superior homonymous quadrantanopia may also occur. Apraxia can be caused by lesions in the parietal lobe, while changes to vision may result from lesions in the occipital lobe. Non-fluent speech can be caused by lesions in the frontal lobe, while ataxia, intention tremor, and dysdiadochokinesia may result from lesions in the cerebellum.

Brain lesions can be localized based on the neurological disorders or features that are present. The gross anatomy of the brain can provide clues to the location of the lesion. For example, lesions in the parietal lobe can result in sensory inattention, apraxias, astereognosis, inferior homonymous quadrantanopia, and Gerstmann’s syndrome. Lesions in the occipital lobe can cause homonymous hemianopia, cortical blindness, and visual agnosia. Temporal lobe lesions can result in Wernicke’s aphasia, superior homonymous quadrantanopia, auditory agnosia, and prosopagnosia. Lesions in the frontal lobes can cause expressive aphasia, disinhibition, perseveration, anosmia, and an inability to generate a list. Lesions in the cerebellum can result in gait and truncal ataxia, intention tremor, past pointing, dysdiadokinesis, and nystagmus.

In addition to the gross anatomy, specific areas of the brain can also provide clues to the location of a lesion. For example, lesions in the medial thalamus and mammillary bodies of the hypothalamus can result in Wernicke and Korsakoff syndrome. Lesions in the subthalamic nucleus of the basal ganglia can cause hemiballism, while lesions in the striatum (caudate nucleus) can result in Huntington chorea. Parkinson’s disease is associated with lesions in the substantia nigra of the basal ganglia, while lesions in the amygdala can cause Kluver-Bucy syndrome, which is characterized by hypersexuality, hyperorality, hyperphagia, and visual agnosia. By identifying these specific conditions, doctors can better localize brain lesions and provide appropriate treatment.

The glossopharyngeal nerve mediates taste and sensation from the posterior one-third of the tongue, while the anterior two-thirds of the tongue receive taste input from the chorda tympani branch of the facial nerve and sensation input from the lingual branch of the mandibular division of the trigeminal nerve. The base of the tongue receives taste and sensation input from the internal branch of the superior laryngeal nerve, which is a branch of the vagus nerve.

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.

The correct diagnosis for a patient presenting with sudden onset vertigo and vomiting, dysphagia, ipsilateral facial pain and temperature loss, contralateral limb pain and temperature loss, and ataxia is posterior inferior cerebellar artery. This constellation of symptoms is consistent with lateral medullary syndrome, also known as Wallenberg syndrome, which is caused by ischemia of the lateral medulla. This condition is associated with involvement of the trigeminal nucleus, lateral spinothalamic tract, cerebellum, and nucleus ambiguus, resulting in the aforementioned symptoms.

The anterior spinal artery, basilar artery, middle cerebral artery, and posterior cerebral artery are not associated with lateral medullary syndrome and would present with different symptoms.

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.

OVALE is a mnemonic that stands for Otic ganglion, V3 (Mandibular nerve: 3rd branch of trigeminal), Accessory meningeal artery, Lesser petrosal nerve, and Emissary veins.

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 abducens nerve.

Anosmia, or loss of smell, can be caused by lesions in the frontal lobe of the brain. In addition to anosmia, frontal lobe lesions may also cause Broca’s aphasia, personality changes, and loss of motor function. Cerebellar lesions, on the other hand, may present with the DANISH symptoms, which include dysdiadochokinesia, ataxia, intention tremor, nystagmus, and hypotonia. Lesions in the occipital lobe can cause visual loss, while lesions in the parietal lobe may cause sensory problems, body awareness issues, and language development weakening. Finally, lesions in the temporal lobe may cause Wernicke’s aphasia, memory loss, emotional changes, and a superior quadrantanopia.

Brain lesions can be localized based on the neurological disorders or features that are present. The gross anatomy of the brain can provide clues to the location of the lesion. For example, lesions in the parietal lobe can result in sensory inattention, apraxias, astereognosis, inferior homonymous quadrantanopia, and Gerstmann’s syndrome. Lesions in the occipital lobe can cause homonymous hemianopia, cortical blindness, and visual agnosia. Temporal lobe lesions can result in Wernicke’s aphasia, superior homonymous quadrantanopia, auditory agnosia, and prosopagnosia. Lesions in the frontal lobes can cause expressive aphasia, disinhibition, perseveration, anosmia, and an inability to generate a list. Lesions in the cerebellum can result in gait and truncal ataxia, intention tremor, past pointing, dysdiadokinesis, and nystagmus.

In addition to the gross anatomy, specific areas of the brain can also provide clues to the location of a lesion. For example, lesions in the medial thalamus and mammillary bodies of the hypothalamus can result in Wernicke and Korsakoff syndrome. Lesions in the subthalamic nucleus of the basal ganglia can cause hemiballism, while lesions in the striatum (caudate nucleus) can result in Huntington chorea. Parkinson’s disease is associated with lesions in the substantia nigra of the basal ganglia, while lesions in the amygdala can cause Kluver-Bucy syndrome, which is characterized by hypersexuality, hyperorality, hyperphagia, and visual agnosia. By identifying these specific conditions, doctors can better localize brain lesions and provide appropriate treatment.