Diagnosing and Managing Headache

Headache is one of the most common symptoms in medicine and a frequent problem in wilderness settings. Its significance ranges from an infrequent and trivial problem to a persistent unpleasant symptom to a marker of serious disease. In wilderness practice, complex headache classifications are of little value.

Headache Mechanisms

Pain receptors are located at the base of the brain in the arteries and veins and throughout the meninges, extracranial vessels, scalp, neck and facial muscles, paranasal sinuses, eyes, and teeth. The brain itself is nearly devoid of pain receptors.

Head pain is mediated via mechanical and chemical receptors, including the stretching of the meninges as well as neurotransmitters such as 5-hydroxytryptamine and histamine and their receptors and pathways. Nerve impulses travel from the peripheral structures above via the fifth and ninth cranial nerves and upper cervical sensory roots, and they pass centrally through the thalamus to the sensory cortex. The vast majority of headaches are benign. However, the diagnostic issue is the question of serious disease.

Common Headache

Almost all headaches without other neurologic signs and with a duration of hours to days are of a band-like or generalized nature, often with a history of some weeks or a background history of several years. These headaches are usually the result of muscle tension or migraine. Migraine associates visual symptoms, nausea, and vomiting with the headaches. Emotional depression is common with any longstanding headache, but it is unwise to assume automatically that a psychological cause lies at the root of a headache.

Headaches are not caused by essential hypertension. Malignant hypertension or accelerated hypertension with hypertensive encephalopathy can cause headache, but this is a rarity.

Eye strain from refractive error does not itself cause headache. New prescription lenses sometimes provoke head pain, which is generally loosely regarded as being the result of eye strain and which is mediated via the pupils readjusting to a new refractive situation.

In wilderness settings in snow, at sea, or in the desert, ultraviolet radiation and glare cause headache. In snow, this is as a part of snowblindness; painful keratoconjunctivitis can develop. Acute mountain sickness is a common cause of headache above 3000 m (9843 feet), and it may be premonitory for HACE. Headache is also said by some to be a feature of dehydration.

Sudden Headache of Short Duration

If pain is focal (e.g., localized to the upper face and lasting minutes to hours), consider sinusitis, glaucoma, and cluster headache. The sudden headache associated with subarachnoid hemorrhage, severe migraine, bacterial meningitis, and cervical arterial dissection is discussed later in this chapter.

Headache Caused by Increased Intracranial Pressure

Intracranial mass lesions displace and stretch the meninges and the basal vessels. Pain is provoked when these structures are shifted either by a mass or by changes in cerebrospinal fluid pressure, such as may be caused by coughing. Cerebral edema around brain tumors causes the further shift of intracranial structures. Pressure headaches typically worsen when a patient is lying down or with movement; this feature is also seen commonly with migraine, acute mountain sickness, and HACE.

Many textbooks indicate that any new headache that is present on waking and made worse by coughing, straining, or sneezing may be the result of a mass lesion, but it should be noted that benign headaches (e.g., migraine) are often made worse with head movement. Vomiting often accompanies pressure headaches. Pressure headaches appear early during the pathologic process and over the course of days or weeks when they are caused by posterior fossa masses or hydrocephalus, but they typically develop over months or years when they are caused by hemisphere tumors. Pressure headaches with ataxia occur with HACE. A rare cause of prostrating headache with lower-limb weakness is an intraventricular tumor that causes intermittent hydrocephalus.

Headache of Subacute Onset

The onset and progression of a headache over days or weeks with or without features of a pressure headache should raise suspicion of an intracranial mass or serious intracranial disease. Encephalitis, viral meningitis, and chronic meningitis should be considered when a headache increases over the course of several days.

Headache with Scalp Tenderness

Patches of exquisite tenderness overlying superficial scalp arteries may be caused by giant cell arteritis (temporal arteritis) in patients who are more than 50 years old, and they almost never appear among younger persons.

Headache after Head Injury

The vast majority of headaches that occur after trauma—even those that last for several months—are not caused by serious intracranial pathology. However, subdural and extradural hematoma (see Chapter 21) must be considered in the aftermath of head injury. Both are rare in the absence of corroborating physical signs.

A Single Episode of Sudden Severe Headache

The common emergency of a single episode of sudden severe headache is caused by migraine or another benign type of headache (e.g., cluster), or it may be the result of serious events such as subarachnoid hemorrhage (SAH), cervical arterial dissection, or the onset of meningitis. The term thunderclap headache is used to describe such a devastating sudden headache without a clear cause. This is usually migrainous, but it also may indicate the onset of subarachnoid bleeding.

Particular attention should be paid to the sudden onset, which is suggestive of SAH. The mode of onset, time to peak, duration, associated symptoms, and the patient’s headache history should be explored. The patient with SAH usually will indicate precisely the time of onset of a sudden headache. High fever, neck stiffness, vomiting, meningeal irritation, and a rash suggest bacterial meningitis, which requires immediate treatment. For nonfebrile persons, careful reassessment over the course of 12 hours can usually sort out whether a sudden headache was a migraine or part of SAH. Bacterial meningitis is often obvious at the onset. Cervical arterial dissection is discussed briefly in this chapter (see Stroke, later).

Classification

The terms that are used to classify epilepsy include idiopathic, symptomatic, cryptogenic, primary generalized, focal (partial), and secondarily generalized. The clinical patterns of the main types of attack are described here.

A generalized (i.e., grand mal or tonic-clonic) seizure is a convulsion that involves bilateral motor manifestations (i.e., convulsive features) and a loss of consciousness. With a primary generalized seizure, the origin of the abnormal electrical spike-and-wave activity seen with electroencephalography during the event is bilateral.

A partial (focal) seizure occurs when the electrical abnormality remains localized to one part of the cerebral cortex. With a simple partial seizure, there is no loss of awareness (e.g., one limb jerking in a Jacksonian seizure). With a complex partial seizure, there is a loss of awareness (e.g., a temporal lobe seizure).

A secondary generalized seizure is a grand mal fit that began as a focal seizure.

Diagnosing a Seizure

Eyewitness accounts may be unclear and colored by the drama of the situation. Some stages of a seizure may be absent. With a primary generalized seizure, the typical stages are first the warning (i.e., a perception that something is about to happen but without a specific aura), which leads to the tonic (i.e., stiff or rigid) phase, during which the patient falls unconscious to the ground, sometimes first uttering a cry. Injuries are common, and the tongue may be severely bitten. Incontinence of urine, feces, or both may follow. The clonic (convulsive) phase begins, with bilateral rhythmic limb jerking and foaming at the mouth. This convulsive phase lasts from a few seconds to several minutes. The patient is typically cyanotic during the attack. Postictal drowsiness, confusion, or coma follows; this sometimes lasts for several hours, but it typically lasts for several minutes.

With a partial seizure, the sequence of events depends on the site of the seizure origin in the cortex. The patient may have an aura before the seizure begins. An aura is a specific and patterned sensation that is caused by a focal cortical electrical discharge.

With a simple Jacksonian partial motor seizure that has its origin within the motor cortex, the patient may sense a vague warning (as with a primary generalized seizure) that is followed by a specific aura (e.g., unusual sensations in one limb). This is followed by the onset of rhythmic jerking, typically in one hand or foot. Jerking spreads to the entire limb or to both the upper and lower limbs and possibly the face on the same side. This progression is known as the “march” of the seizure. Consciousness is not lost during a simple partial seizure. In place of postictal drowsiness or coma, weakness of the limbs that were involved with the seizure may follow. This is known as Todd’s paralysis, and it may last for several hours. A stroke may be suspected if early stages of the seizure were not witnessed or if they are unclear.

With a complex partial seizure of temporal lobe origin, the patient may experience an aura of familiarity with his or her surroundings, which is known as déjà vu; this is followed by an “absence attack” during which the patient is generally unaware or disoriented. As the seizure develops, the patient looks distant (i.e., appears to be in a trance-like state) and does not respond to stimuli. Facial or lip twitching may occur. Recovery is typically rapid, with the patient regaining full awareness in a matter of seconds or minutes (and rarely in more than 10 minutes).

A focal seizure may progress to become secondarily generalized. For example, a Jacksonian motor seizure may develop into a grand mal fit.

The usual differential diagnosis of a seizure is between syncope and a nonepileptic attack. There are many causes of loss of consciousness or sudden attacks; these are described later in this chapter. Assuming that one knows what to expect, they are usually recognizable.

Emergency Management of Seizures

In the field, a seizure may well take place in a sensational situation, such as on a glacier, on a steep path, on a climb, or at sea. The doctor’s actions are frequently very much in the public view, and there is often an expectation that skilled and urgent treatment must be seen to be underway. The reality is that careful observation is usually the most important activity.

Immediately establish and maintain a patent airway. Do not force the patient’s mouth open. Wooden mouth wedges, tongue forceps, and excessive restraint are likely to cause more injuries than will any seizure. Deep cyanosis is typical during a grand mal fit. The spontaneous return of normal breathing and oxygenation will remedy the problem.

If an attack lasts for more than a few seconds, stay with the patient, summon help, assist with breathing, and establish intravenous access, if possible. The latter is unlikely to be necessary, but it prepares the patient for the medical emergency of status epilepticus. Most seizures resolve spontaneously.

Managing A Probable First-Time Seizure

Although no hard-and-fast rules can be laid down, a definite unprovoked first grand mal seizure is usually sufficient reason to evacuate a patient. However, even in this situation, the yield of investigation is low, and the tendency exists to overdiagnose epilepsy. Often, despite a good history from an eyewitness, one may remain in some doubt about the nature of an attack. When there is uncertainty, it is useful to recall the benign outcome of the majority of blackouts and to remember that it may be reasonable to await events. It is usually prudent to not use antiepileptic drugs until a diagnosis of epilepsy is certain, despite pressure from either the patient or his or her team members to administer them.

Simple Syncope, Cardiac Syncope, Postural Hypotension, and Drop Attacks

Fainting is the result of sudden reflex bradycardia with vasodilatation of peripheral and splanchnic vasculature. This is simple syncope, which is also known as neurocardiogenic syncope, and it is a common response to prolonged standing, fear, venipuncture, or pain. Syncope almost never occurs when an individual is in the recumbent posture, unless the vagal response is profound. The subject falls to the ground and is unconscious for less than 2 minutes, and recovery is rapid. Jerking movements may occur, especially if the patient is trapped in a sitting position; this can briefly resemble a grand mal seizure. Incontinence of urine may occur.

Cardiac syncope caused by arrhythmia is potentially serious and often treatable. Typically the onset is abrupt and involves pallor and an irregular or nonpalpable pulse. Asystole or ventricular tachycardia generally causes cardiac syncope. A useful working rule in the field is that supraventricular tachycardias are usually obvious to the patient as palpitations and light-headedness, and they rarely produce loss of consciousness.

Syncope can occur after micturition in men, particularly at night, and in either sex when venous return to the heart is obstructed by breath holding and severe coughing. “Effort syncope” is of cardiac origin.

Postural hypotension is also a cause of syncope. This typically occurs among the elderly, among those with autonomic neuropathy, and as a result of the effects of phenothiazines, levodopa, or tricyclic antidepressants. Postural hypotension symptoms also occur during acclimatization to altitude.

Carotid sinus problems can occasionally cause syncope, but these are difficult to diagnose. Syncope can also occur with severe anemia and blood loss.

Drop Attacks and Hydrocephalus

Drop attacks are sudden-onset, unexpected episodes of lower-limb weakness with falling that occur primarily among women who are more than 60 years old. Awareness is preserved. There is a sudden unprovoked loss of lower-limb tone that is presumably of brainstem origin. Patients are frequently injured. Sudden attacks of leg weakness may also occur with hydrocephalus, presumably as a result of brainstem compression.

Syncope: Management

The immediate management of syncope or impending syncope is to lay the patient down, lift the patient’s legs, and record the pulse. For the rare circumstances in which brain blood flow cannot be restored (e.g., when a person is propped upright in a chair), brain infarction can follow syncope.

Syncope in its various forms can usually be distinguished from epilepsy. Witnessed accounts are invaluable. Postepisode confusion with amnesia suggests a seizure, as do foaming at the mouth and substantive tongue biting. Pallor is typical with syncope.

Other Causes of Sudden Attacks and “Funny Turns”

Pseudoseizure is mentioned first because it is common during stressful situations. There are no truly diagnostic features of pseudoseizures. However, immediate loss of consciousness without a prelude that is followed by bizarre flailing limb movements that do not look truly convulsive are most common. Cyanosis is rare, and frothing at the mouth unusual. Pseudoseizure can be a difficult diagnosis, and status epilepticus can be successfully mimicked.

Sleep Management

Meningitis

Bacterial infections within the nervous system pose difficult dilemmas in any setting, but they require a particularly pragmatic approach when one is far from help. Bacterial meningitis is fatal unless it is treated promptly. Bacterial meningitis may be difficult to distinguish from self-limited viral infection.

Microorganisms reach the meninges either by direct extension from the ears or nasopharynx, as a result of cranial injury or congenital defect, or via the bloodstream. Patients who are at particular risk are those with compromised immune systems.

With acute bacterial meningitis, the pia-arachnoid becomes congested with neutrophils, and a thin layer of pus forms. Pus can organize to form adhesions that lead to cranial nerve palsies and hydrocephalus. With chronic infection (typically with tuberculosis), the brain surface becomes covered in sticky grey-green exudate with numerous meningeal tubercles. Adhesions are invariable. Brain edema occurs with any bacterial meningitis.

The Meningitic Syndrome

The classic diagnostic triad for meningeal irritation is headache, stiff neck, and fever. With acute bacterial meningitis, there are usually intense malaise, fever, rigors, headache, photophobia, and vomiting that develop within hours or even minutes of infection. The patient is irritable and prefers to lie still. Neck stiffness and a positive Kernig’s sign (i.e., neck and back pain when the hip and knee are flexed with the patient supine) usually appear within hours. Brudzinski’s sign (i.e., spontaneous flexion of hips and knees when the neck is flexed with the patient supine) may also be present.

The diagnostic conundrum is that sometimes with bacterial meningitis there are few prominent meningitic features, and the clinical picture may resemble viral meningitis. For example, neck stiffness may not be evident. A mild form of the meningitic triad is reliable as an indicator of meningeal irritation but not of its cause. If in doubt, treat the patient for bacterial meningitis.

Clues to Specific Varieties of Bacterial Meningitis

Possible infecting organisms are shown in Table 33-1. However, in wilderness practice, treatment for an unknown pyogenic organism will be required.

TABLE 33-1 Some Clinical Clues to Meningitis

Emergency Wilderness Management of Meningitis

If acute bacterial meningitis is suspected, treatment must be started immediately and before evacuation is even considered.

Table 33-2 indicates a practical treatment approach, but it is important that up-to-date information about treatment protocols, potential allergies, and drug side effects is sought before embarking for a remote area.

TABLE 33-2 Antibiotics for the Treatment of Possible Acute Bacterial Meningitis

* Dosing information for these medications can be found in the text of this chapter.IV, Intravenously.

Doses from Clarke C, Howard R, Shorvon S, et al: Neurology: A Queen Square textbook, Oxford, UK, 2009, Wiley Blackwell Publishing, p. 292.

Evidence suggests that the administration of steroids (e.g., 10 mg of intravenous dexamethasone very 6 hours for 4 days) commencing with the first antibiotic dose reduces complications such as brain edema and delayed deafness.

Viral, Subacute, and Chronic Meningitis and Encephalitis

Most cases of viral meningitis begin to improve after several days. Meningitis that has a more chronic course (e.g., with neck stiffness and drowsiness over several days or weeks) may be caused by tuberculosis, another chronic meningeal infection (e.g., cryptococcus, brain abscess, encephalitis), or a general medical condition (e.g., endocarditis). Evacuation will usually be required in these situations.

Diagnosis of Transient Ischemic Attack

TIAs cause a sudden loss of function, usually within seconds and without a prelude. By definition, they last less than 24 hours, and they usually last only minutes or hours at most (Table 33-3).

TABLE 33-3 Features of Transient Ischemic Attacks

There is usually no difficulty distinguishing TIA from a focal seizure, because TIA symptoms are usually negative in the sense that there is weakness, visual loss, or aphasia; alternatively, epileptic events cause convulsive movements. Positive visual symptoms (e.g., lights, flashes) and headache point to migraine.

Amaurosis fugax, which is defined as a sudden loss of vision in one eye that lasts minutes to hours, can be caused by thromboembolism. For circumstances in which an episode has been witnessed, arterial emboli have been seen to pass through the retinal circulation. Amaurosis fugax also occurs as a migraine phenomenon.

An episode of isolated loss of consciousness is rarely if ever caused by TIA. Transient global amnesia or a sudden loss of memory and orientation that lasts minutes to hours is usually not a prelude to stroke and is excluded as a form of TIA.

Managing Transient Ischemic Attack and Stroke

Thorough vascular and cardiac examinations are essential. After a TIA, there are no abnormal neurologic signs. After a stroke, hemiplegia (i.e., profound, total weakness) and aphasia may be evident, or there may be a less severe residual deficit (e.g., hemiparesis).

Transient Ischemic Attack and Stroke in Special Circumstances

Sudden neurologic events occur after underwater dives and at high altitude. Diving problems, decompression sickness, and the dangers of syncopal episodes after shallow dives are discussed in Chapter 77.

There are numerous case reports of TIA and stroke-like events occurring at altitudes of more than 5000 m (16,404 feet), some in the setting of HACE and others presumably brought on by dehydration and polycythemia caused by chronic hypoxia.

With HACE, a stroke-like event may be the first sign of brain edema, and it may occur out of the blue in well-acclimatized climbers at extreme altitudes (i.e., usually above 6500 m [21,325 feet]). This is in contrast with the typical cases of HACE that occur at around 5000 m (16,404 feet) with headaches and ataxia, when there is an apparent failure of acclimatization. Papilledema in a well-acclimatized man at 7600 m (24,934 feet) with sudden ataxia is illustrated in Figure 33-2.

FIGURE 33-2 Papilledema in a sherpa climbing at 7600 m (24,934 feet) on Mt Everest’s southwest face in 1975. Photo taken at 6100 m (20,013 feet).

(Courtesy Dr. Charles Clarke.)

Transient TIA-like episodes of aphasia, visual disturbances, and unilateral weakness are also well described, again mostly at extreme altitudes above 6500 m (21,325 feet).

Climbing expedition physicians have performed therapeutic phlebotomy to reduce polycythemia in these situations, which is a reasonable enough practice if it can be performed safely. One withdraws one-half a liter of blood and replaces it with normal saline, with the entire process occurring over the course of 4 hours.

Median Nerve Compression at the Wrist: Carpal Tunnel Syndrome

This common cause of nocturnal tingling in the hands is in a median nerve distribution and involves clumsiness with weakness, typically of thumb movements (e.g., when opening bottles). It is less well known that pain in the forearm is often prominent and that numbness may extend above the wrist or be rather vague and poorly localized. Weakness of the abductor pollicis brevis (i.e., moving the thumb at right angles to the palm) is the earliest motor sign.

A wrist splint that holds the wrist in slight extension at night is helpful. Elevation of the arm at night also helps, but this may not be feasible in a tent. Steroid injection into the wrist along the median nerve is not a simple or risk-free procedure. If symptoms persist long term, nerve conduction studies should be advised on return. Surgical carpal tunnel decompression is almost always curative, but it is certainly not meant to occur in the outback.

Ulnar Nerve Compression at the Elbow

Transient tingling in an ulnar nerve distribution is almost universal in uncomfortable beds, and it is of little importance. However, persistent tingling that progresses to a weakness of finger abduction implies substantial compression of the ulnar nerve at the elbow. This may resolve with the use of an elbow splint and elbow pads and by avoiding leaning on the elbows; however, after it has been established for more than a week, it may require surgical ulnar nerve decompression and transposition.

Radial Nerve Palsy: Compression in the Spiral Groove of the Humerus

The radial nerve lesion known as Saturday night palsy is typically caused when an individual falls asleep with one arm draped over a hard chair. The patient awakes thinking that he or she may have had a stroke. Weakness of wrist and finger extension causes profound disability, but there is typically little or no sensory loss. Weakness almost always resolves spontaneously in about 3 to 6 weeks.

Backpacks: Numb Hands, Backpack Palsy, and Neurogenic Thoracic Outlet Syndrome

Transient numb and weak hands occur when rucksack shoulder straps are too tight or when a load is too heavy. Symptoms usually resolve within a few days, but occasionally there occurs damage to a branch of the brachial plexus. It is often hard to determine the precise nerve that has been affected. True rucksack or backpack palsy was first described as being caused by the compression of the long thoracic nerve. This is a rarity that causes weakness of the serratus anterior muscle and leads to a “winged” scapula, which is diagnosed when the patient pushes the palm of each hand against a wall; the weak scapula protrudes from the back.

Neurogenic thoracic outlet syndrome is a C8 or T1 nerve root lesion caused by a cervical rib or a fibrous band that can become symptomatic as a result of compression by a backpack strap above the clavicle.

Thigh Pain and Tingling: Meralgia Paresthetica

Painful tingling of the outer thigh in the distribution of the lateral cutaneous (femoral) nerve of the thigh is common, especially among persons who are obese. It is also sometimes seen when the thigh swells after strenuous exercise. The problem usually resolves over a few days, and no treatment is necessary.

Foot Drop: Peroneal and Sciatic Nerve Lesions

Peroneal (lateral popliteal) nerve palsy is the third most common focal motor neuropathy, after compression of the median and ulnar nerves. The peroneal nerve is compressed behind the head of the fibula at the knee. There is foot drop, which is usually noticed after an unusual posture such as squatting. There is profound weakness of the tibialis anterior, extensor hallucis longus, and peroneal muscles. The patient cannot dorsiflex and evert the ankle or extend the great toe. Deep tendon reflexes remain intact. The small patch of numbness above the lateral malleolus is often barely noticeable. The usual course is one of spontaneous recovery over a few weeks. An ankle splint that supports the foot comfortably at a right angle to the tibia may be useful. This cause of foot drop needs to be distinguished from anterior compartment syndrome, which is a surgical emergency.

Sciatic nerve palsy, which is caused by pressure in the gluteal region or a misplaced intramuscular injection, causes weakness of the hamstrings and of all muscles below the knee. Transient minor sciatic palsy is the “dead leg” that results from sitting on the edge of an uncomfortable chair and that resolves within minutes. By contrast, established sciatic nerve lesions tend to remain painful.

Lumbar Back Pain: Lateral and Central Disc Protrusion

Acute low back pain of disc or facet origin is common, and it is discussed in Chapter 21. One valuable emergency treatment is gentle spinal manipulation if pain and circumstances allow. My preferred method is to lay the patient supine on a firm, flat surface. Examine the patient neurologically, and check hip, knee, and ankle joint movements. Sitting astride the supine patient, grasp one knee and thigh in a firm but gentle elbow lock. Firmly flex and rotate the hip so that the patient’s flexed knee, which is held in your elbow, points toward the opposite hip of the patient. Although this is primarily a treatment for facet joint problems, it is generally worth trying. Keep all patients with back pain active if at all possible.

Lateral lumbar disc protrusion typically causes an L5 or S1 nerve root lesion. There is acute low back pain, sciatica, and a limitation of straight-leg raising. The ankle jerk is lost with an S1 lesion. With an L5 lesion, extension of the great toe becomes weak. The usual course, even when there is substantial weakness, is for spontaneous recovery that occurs over days to weeks. When weakness is progressive, emergency surgery may be required, so evacuation is advisable.

Central lumbosacral disc protrusion is a distinctly uncommon surgical emergency. Back pain is followed by sacral and perineal numbness and flaccid weakness of the lower limbs, usually for several hours, with the retention of urine; this is known as cauda equina syndrome. Even with prompt surgery, many of these patients have residual deficits and thus should be evacuated.

Cervical Disc Lesions

Acute neck pain is covered in Chapter 21. The potential neurologic sequelae of degenerative cervical disc disease are lateral disc protrusion that causes a cervical root lesion and central disc protrusion that causes spinal cord compression and paraparesis. Lateral cervical disc protrusion can be intensely painful, but it is usually self-limited. Central cervical disc protrusions are frequently painless, may cause no neck symptoms, and are usually progressive; they require urgent specialist treatment.

Acute Lateral Cervical Disc Protrusion

Sudden pain in the neck and down the arm is typical with acute lateral cervical disc protrusion, and neck movement is restricted. Pain may be excruciating and require opiate analgesia. The C7 root is most commonly affected. Root pain radiates to the myotome—in this case, the triceps, muscles deep to the scapula, and the forearm extensors, all of which may be weak—with tingling and numbness in the C7 dermatome, which includes the middle finger. The triceps reflex is also lost.

Lay the patient down, and immobilize his or her neck. An inflatable or makeshift neck splint prevents neck motion. Check that all passive upper-limb joint movements are free, and keep exercising the upper limb passively several times daily to prevent stiffness and potential frozen shoulder. The acute pain, which may be intense and require opiates, usually resolves within 1 week. During the days before imaging, these cases would usually only be investigated after several weeks. A minority of these patients require surgery.

Neuralgic Amyotrophy (Acute Brachial Neuritis)

This intensely painful condition, which is presumed to be an acute demyelinating brachial plexopathy with an allergic basis, is mentioned because it is frequently misdiagnosed as an acute cervical root lesion. Severe acute pain develops around the shoulder girdle, and is followed by weakness and wasting of the supraspinatus, infraspinatus, deltoid, and serratus anterior muscles, all during the course of a week. Gradual resolution over many months is the rule. Pain may require the administration of opiates. Steroids (e.g., 50 mg of prednisolone for 5 days) are often given, although there is little evidence base for this therapy.

Central Cervical Disc Protrusion (Cervical Myelopathy), Cord Compression, and Paraparesis

The typical presentation of a central cervical disc compressing the spinal cord is of ascending lower-limb numbness, spasticity, and weakness with loss of bladder control. Spastic paraparesis implies possible spinal cord compression, which is a potential neurosurgical emergency. Although there are many causes of spastic paraparesis, precise diagnosis is impossible in a wilderness setting. Evacuation will usually be mandatory.

Cranial Nerve Palsies and Vertigo

Cranial nerve VII is by far the most commonly affected, and this is manifested as Bell’s palsy, described later.

Loss of the sense of smell is sometimes a sequel to upper respiratory infection. If that is the cause, the ability to smell returns over a few weeks. Anosmia as a result of severance of the olfactory nerves as they pierce the cribriform plate can follow head injury and become permanent.

A lesion of any other single cranial nerve usually merits specialist investigation, but this is seldom a neurologic emergency. One exception that requires urgent investigation is a painful oculomotor nerve palsy, when the eye points down and out with a pupil that is large and fixed. Aneurysm of the posterior communicating artery is the diagnosis until proved otherwise.

Visual failure is discussed in Chapter 28.

Epilepsy

Well-controlled epilepsy should not be a bar to wilderness activity. The general risk assessment must include the question of danger to the patient as well as to other members of the party. Rock climbing, sea kayaking, and diving (other than snorkeling in company) are usually prohibited. For example, when a patient with a history of seizures is assessed for suitability to join a trek at altitudes of 4500 to 5500 m (14,764 to 18,045 feet), consider the following:

There is no evidence that seizures are provoked by exercise, acute mountain sickness, or cerebral edema.

Cerebrovascular Disease

Hypertension that is well controlled at home usually remains so in wilderness settings and at altitude. Patients who have recovered well after ischemic or hemorrhagic stroke do not appear to be at any increased risk. I know of several cases of professional mountaineers who have returned to climbing after recovery from a minor stroke.

In my experience, two areas cause particular difficulty. One is the applicant to an expedition who may have had a previous TIA. Some difficulties with reaching a diagnosis have been outlined previously. My advice and practice are as follows:

A second specific situation relates to a previous TIA-like event that has taken place at high altitude (usually over 7000 m [22,966 feet]). This quandary is not uncommon, and examples include transient hemiparesis or aphasia on a previous expedition. Should the patient once again travel to a high altitude? Such events can be caused by hyperviscosity, by incipient brain edema, or occasionally by thromboembolism, or they may have a benign cause such as migraine.