Nerve Injuries and Clinical Features: A Guide

The human body is a complex system of nerves and muscles, and injuries to these structures can have a significant impact on daily life. Here is a guide to some common nerve injuries and their associated clinical features.

Common Peroneal Nerve at the Head of the Fibula
The common peroneal nerve is often damaged as it wraps around the fibular head. This can result in foot drop, weak dorsiflexion and eversion of the foot, weak extension of the toes, sensory loss over the dorsum of the foot and lateral side of the leg, and intact reflexes.

Common Peroneal Nerve at the Ankle
The common peroneal nerve bifurcates into two terminal branches shortly after passing over the fibular head. Damage to one of these branches can occur at the ankle, but not to the common peroneal nerve itself. Symptoms may include sensory loss and weakness in the affected area.

Sciatic Nerve at the Sciatic Notch
Injury to the sciatic nerve at this level can result in pain down the thigh, loss of sensation to the whole leg below the knee (except for a narrow area on the medial leg and medial foot border), widespread motor deficit, and foot drop. The ankle jerk is lost.

Tibial Nerve at the Popliteal Fossa
Damage to the tibial nerve at this level can lead to gastrocnemius paralysis, weakened inversion and plantar flexion at the ankle, and loss of the ankle jerk. This type of injury is relatively uncommon.

Tibial Nerve at the Ankle
Compression of the tibial nerve at the level of the medial malleolus can result in tarsal tunnel syndrome. Symptoms may include paraesthesiae or numbness affecting the medial ankle and plantar aspect of the foot, weakness to the toe abductors and flexors, and tenderness at the medial malleolus. Foot drop is not a feature.

In summary, nerve injuries can have a range of clinical features depending on the location and severity of the damage. It is important to seek medical attention if you suspect you have sustained a nerve injury.

It is unlikely that the patient experienced a stroke as her symptoms resolved completely after 10 minutes and there were no ongoing symptoms. Different types of strokes affect different arteries in the brain. For example, a lesion in the anterior cerebral artery would result in contralateral hemiparesis and sensory loss, with the lower extremities being more affected than the upper. On the other hand, a lesion in the posterior cerebral artery would cause contralateral homonymous hemianopia with macular sparing. If the posterior inferior cerebellar artery is affected, the patient may experience ipsilateral facial pain and temperature loss, as well as contralateral limb and torso pain and temperature loss, along with ataxia and nystagmus. A middle cerebral artery stroke would cause contralateral hemiparesis and sensory loss, with the upper extremity being more affected than the lower, as well as contralateral homonymous hemianopia and aphasia.

When a stroke occurs, the location of the lesion in the brain can determine the specific effects on the body. Depending on which artery is affected, different symptoms may arise. For example, a stroke in the anterior cerebral artery can lead to contralateral hemiparesis and sensory loss, with the lower extremity being more affected than the upper. On the other hand, a stroke in the middle cerebral artery can cause contralateral hemiparesis and sensory loss, with the upper extremity being more affected than the lower, as well as contralateral homonymous hemianopia and aphasia.

If the stroke occurs in the posterior cerebral artery, the individual may experience contralateral homonymous hemianopia with macular sparing and visual agnosia. In the case of Weber’s syndrome, which involves branches of the posterior cerebral artery that supply the midbrain, the person may have an ipsilateral CN III palsy and contralateral weakness of the upper and lower extremities.

Other types of strokes include those affecting the posterior inferior cerebellar artery, which can lead to ipsilateral facial pain and temperature loss and contralateral limb/torso pain and temperature loss, as well as ataxia and nystagmus. A stroke in the anterior inferior cerebellar artery can cause similar symptoms to Wallenberg’s syndrome, but with the addition of ipsilateral facial paralysis and deafness.

Finally, lacunar strokes are small, localized strokes that often occur in individuals with hypertension. They typically present with isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia, and commonly affect the basal ganglia, thalamus, and internal capsule.

Understanding Different Types of Headaches

Headaches are a common ailment that can be caused by a variety of factors. Here are some of the different types of headaches and their distinguishing characteristics:

1. Tension headache: This type of headache is often described as a tight, band-like pain across the forehead and is more common in females. It typically worsens towards the end of the day but does not interfere with daily activities. Chronic tension headaches occur at least 15 days of the month for at least three months.

2. Brain tumour: Headaches caused by space-occupying lesions tend to be worse in the morning and when bending forward. They may also be associated with vomiting.

3. Cluster headache: This type of headache is more common in men and presents with intense pain localized around one eye, which can last for a few minutes up to three hours. There may also be simultaneous lacrimation and nasal congestion. Symptoms occur every day or multiple times every day for a number of weeks, followed by a symptom-free period lasting months or even years.

4. Giant cell arteritis: This type of headache typically occurs in those aged over 50 years and is characterized by an abrupt onset and recurrent daily headache. Common symptoms include scalp pain/tenderness, jaw claudication, visual disturbances, fever, weight loss, and lethargy. A diagnosis of GCA requires three out of five specific criteria.

5. Migraine: Migraines can occur daily but are typically accompanied by associated features such as nausea or vomiting, photophobia, or phonophobia. The International Headache Society criteria for migraine without aura include at least five attacks fulfilling specific criteria.

Understanding the different types of headaches and their characteristics can help in proper diagnosis and treatment.

For the prophylactic management of migraines in a patient with a history of asthma, the recommended medication is topiramate. Propranolol is an alternative first-line option, but should be avoided in patients with asthma. Amitriptyline is a second-line drug for those who are not responsive to initial prophylactic treatment. Diclofenac is an NSAID used for acute management of migraines, while triptans like sumatriptan are used for acute treatment but not prophylaxis. It should be noted that topiramate is teratogenic and should be avoided in women of childbearing age.

Managing Migraines: Guidelines and Treatment Options

Migraines can be debilitating and affect a significant portion of the population. To manage migraines, it is important to understand the different treatment options available. According to the National Institute for Health and Care Excellence (NICE) guidelines, acute treatment for migraines involves a combination of an oral triptan and an NSAID or paracetamol. For young people aged 12-17 years, a nasal triptan may be preferred. If these measures are not effective, non-oral preparations of metoclopramide or prochlorperazine may be considered, along with a non-oral NSAID or triptan.

Prophylaxis should be given if patients are experiencing two or more attacks per month. NICE recommends topiramate or propranolol, depending on the patient’s preference, comorbidities, and risk of adverse events. Propranolol is preferred in women of childbearing age as topiramate may be teratogenic and reduce the effectiveness of hormonal contraceptives. Acupuncture and riboflavin may also be effective in reducing migraine frequency and intensity for some people. For women with predictable menstrual migraines, frovatriptan or zolmitriptan may be recommended as a type of mini-prophylaxis.

Specialists may consider other treatment options, such as candesartan or monoclonal antibodies directed against the calcitonin gene-related peptide (CGRP) receptor, like erenumab. However, pizotifen is no longer recommended due to common adverse effects like weight gain and drowsiness. It is important to exercise caution with young patients as acute dystonic reactions may develop. By following these guidelines and considering various treatment options, migraines can be effectively managed.

When a patient shows symptoms of acute stroke, it is crucial to immediately send them to the nearest stroke center. Treatment should not be administered until a diagnosis of ischemic stroke is confirmed. Once confirmed, the patient should be prescribed aspirin 300 mg daily for two weeks, followed by long-term use of clopidogrel 75 mg daily. Additionally, if the patient is not already taking a statin, it should be offered as a treatment option.

The Royal College of Physicians (RCP) and NICE have published guidelines on the diagnosis and management of patients following a stroke. The management of acute stroke includes maintaining normal levels of blood glucose, hydration, oxygen saturation, and temperature. Blood pressure should not be lowered in the acute phase unless there are complications. Aspirin should be given as soon as possible if a haemorrhagic stroke has been excluded. Anticoagulants should not be started until brain imaging has excluded haemorrhage. Thrombolysis with alteplase should only be given if administered within 4.5 hours of onset of stroke symptoms and haemorrhage has been definitively excluded. Mechanical thrombectomy is a new treatment option for patients with an acute ischaemic stroke. NICE recommends thrombectomy for people who have acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography or magnetic resonance angiography. Secondary prevention includes the use of clopidogrel and dipyridamole. Carotid artery endarterectomy should only be considered if carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.

Verapamil is utilized to prevent cluster headaches in the long term, while sumatriptan is employed as an immediate rescue therapy in conjunction with high-flow oxygen. It is important to carefully read the question to ensure the correct medication is selected. Propranolol is used for migraine prevention, while sertraline, an SSRI, is used to treat depression and has a similar mechanism of action to sumatriptan.

Cluster headaches are a type of headache that is known to be extremely painful. They are called cluster headaches because they tend to occur in clusters that last for several weeks, usually once a year. These headaches are more common in men and smokers, and alcohol and sleep patterns may trigger an attack. The pain typically occurs once or twice a day, lasting between 15 minutes to 2 hours. The pain is intense and sharp, usually around one eye, and is accompanied by redness, lacrimation, lid swelling, and nasal stuffiness. Some patients may also experience miosis and ptosis.

To manage cluster headaches, 100% oxygen or subcutaneous triptan can be used for acute treatment, with response rates of 80% and 75% respectively within 15 minutes. Verapamil is the drug of choice for prophylaxis, and a tapering dose of prednisolone may also be effective. It is recommended to seek specialist advice from a neurologist if a patient develops cluster headaches, especially with respect to neuroimaging. Some neurologists use the term trigeminal autonomic cephalgia to group a number of conditions including cluster headache, paroxysmal hemicrania, and short-lived unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT). Patients with these conditions should be referred for specialist assessment as specific treatment may be required, such as indomethacin for paroxysmal hemicrania.

Immediate CT scan is necessary to evaluate for raised intracranial pressure and tentorial herniation in a patient with a sluggishly responsive unilaterally dilated pupil. This is the most pressing concern, given the patient’s reduced GCS. Although other investigations will be necessary, the CT brain is the most critical test, as the patient may require urgent neurosurgical intervention to save their life.

Patients with head injuries should be managed according to ATLS principles and extracranial injuries should be managed alongside cranial trauma. There are different types of traumatic brain injuries, including extradural hematoma, subdural hematoma, and subarachnoid hemorrhage. Primary brain injury may be focal or diffuse, and secondary brain injury can occur due to cerebral edema, ischemia, infection, or herniation. Management may include IV mannitol/frusemide, decompressive craniotomy, and ICP monitoring. Pupillary findings can provide information on the location and severity of the injury.

Bell’s palsy affects the lower motor neurons and results in weakness of the entire side of the face. A left cranial nerve VII lower motor neuron lesion would cause left-sided facial weakness without forehead sparing. However, lateral medullary syndrome, caused by ischemia to the lateral medulla oblongata, would present with vertigo, dizziness, nystagmus, ataxia, nausea and vomiting, and dysphagia. A left cranial nerve VII upper motor neuron lesion would result in right-sided facial weakness with forehead sparing, while a right cranial nerve VII lower motor neuron lesion would cause right-sided facial weakness without forehead sparing.

Understanding Bell’s Palsy

Bell’s palsy is a sudden, one-sided facial nerve paralysis of unknown cause. It is more common in individuals aged 20-40 years and pregnant women. The condition is characterized by lower motor neuron facial nerve palsy, which affects the forehead. Unlike upper motor neuron lesions, the upper face is spared. Patients may also experience post-auricular pain, altered taste, dry eyes, and hyperacusis.

The management of Bell’s palsy has been a subject of debate. However, it is now widely accepted that all patients should receive oral prednisolone within 72 hours of onset. The addition of antiviral medications is still a matter of discussion, but it may be beneficial for severe facial palsy. Eye care is also crucial to prevent exposure keratopathy, and patients should be prescribed artificial tears and eye lubricants. If they are unable to close their eyes at bedtime, they should tape them closed using microporous tape.

If the paralysis shows no sign of improvement after three weeks, an urgent referral to ENT is necessary. Patients with long-standing weakness may require a referral to plastic surgery. The prognosis for Bell’s palsy is generally good, with most patients making a full recovery within 3-4 months. However, untreated patients may experience permanent moderate to severe weakness in around 15% of cases.

To minimize the risk of errors, brain death testing must be conducted by two experienced doctors on different occasions. The testing involves evaluating the patient’s history, pupil reactions, reflexes, pain response, and respiratory effort. Once brain death is confirmed, life support can be discontinued, and the patient may be considered for organ donation, which can take place before the withdrawal of life support.

Criteria and Testing for Brain Stem Death

Brain death occurs when the brain and brain stem cease to function, resulting in irreversible loss of consciousness and vital functions. To determine brain stem death, certain criteria must be met and specific tests must be performed. The patient must be in a deep coma of known cause, with reversible causes excluded and no sedation. Electrolyte levels must be normal.

The testing for brain stem death involves several assessments. The pupils must be fixed and unresponsive to changes in light intensity. The corneal reflex must be absent, and there should be no response to supraorbital pressure. The oculo-vestibular reflexes must be absent, which is tested by injecting ice-cold water into each ear. There should be no cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation. Finally, there should be no observed respiratory effort in response to disconnection from the ventilator for at least five minutes, with adequate oxygenation ensured.

It is important that the testing is performed by two experienced doctors on two separate occasions, with at least one being a consultant. Neither doctor can be a member of the transplant team if organ donation is being considered. These criteria and tests are crucial in determining brain stem death and ensuring that the patient is beyond recovery.

The correct answer is cubital tunnel syndrome. This condition is characterized by ulnar nerve neuropathy, which affects the sensory innervation of the palmar and dorsal aspects of 1.5 fingers medially. It can also cause wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals) and the hypothenar muscles. To test for ulnar neuropathy, Froment’s test can be used to assess the function of the adductor pollicis muscle.

Axillary nerve neuropathy is not the correct answer. The axillary nerve has both motor and sensory functions, innervating the deltoid and teres minor muscles, as well as providing sensory innervation to the skin over the lower two-thirds of the posterior part of the deltoid and the long head of the triceps brachii.

C8/T1 radiculopathy is also not the correct answer. While it can mimic ulnar nerve neuropathy, the preserved sensation of the forearm would suggest cubital tunnel syndrome instead. The medial antebrachial cutaneous nerve (C8 and T1) provides sensation to the medial forearm, not the ulnar nerve.

Carpal tunnel syndrome is also not the correct answer. This condition is caused by median nerve dysfunction, resulting in sensory loss over the lateral 3.5 digits and loss of motor function to the flexor muscles of the forearm and hand, as well as those responsible for thumb movement.

The Ulnar Nerve: Overview, Branches, and Patterns of Damage

The ulnar nerve is a nerve that arises from the medial cord of the brachial plexus, specifically from the C8 and T1 spinal nerves. It provides motor innervation to several muscles in the hand, including the medial two lumbricals, adductor pollicis, interossei, hypothenar muscles (abductor digiti minimi, flexor digiti minimi), and flexor carpi ulnaris. It also provides sensory innervation to the medial 1 1/2 fingers on both the palmar and dorsal aspects.

The ulnar nerve travels through the posteromedial aspect of the upper arm before entering the palm of the hand via the Guyon’s canal, which is located superficial to the flexor retinaculum and lateral to the pisiform bone. The nerve has several branches, including the muscular branch, palmar cutaneous branch, dorsal cutaneous branch, superficial branch, and deep branch. These branches supply various muscles and skin areas in the hand.

Damage to the ulnar nerve can occur at the wrist or elbow. When damaged at the wrist, it can result in a claw hand deformity, which involves hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits. There may also be wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals) and hypothenar muscles, as well as sensory loss to the medial 1 1/2 fingers. When damaged at the elbow, the same symptoms may occur, but with the addition of radial deviation of the wrist. It is important to note that in distal lesions, the clawing may be more severe, which is known as the ulnar paradox.