Headache
Headache is a common complaint and does not usually indicate serious disease. In most patients presenting with headache there are no abnormal physical signs and the diagnosis depends upon an accurate history. The causes of headache can be broadly divided according to their onset and subsequent course (Table 17.1). The underlying causes of acute or subacute onset of headache are all potentially serious and require urgent investigation and assessment. Subarachnoid haemorrhage presents with headache which reaches maximum intensity within seconds of onset and is described as the ‘worst ever' (p. 750). Neck stiffness and a positive Kernig's sign indicate meningeal irritation, which usually occurs because of bacterial or viral men-ingitis, or subarachnoid haemorrhage. Fever may also occur with these conditions.
The history and physical examination are the keys to distinguishing serious from benign causes of headache in patients with chronic or recurrent head-ache; most are due to tension-type headache (p. 774) and do not require further investigation. Progressively worsening headaches, or chronic head-aches that change in character, may be caused by raised intracranial pres-sure, e.g. due to a space-occupying lesion, and require brain imaging by CT scan or MRI. Other features which indicate a higher risk of serious pathology and are indications for imaging are listed in Table 17.2. Headache with generalized aches and pains in the elderly suggests giant cell arteritis which requires urgent treatment with steroids to prevent blindness (p. 777).
Dizziness, faints and ‘funny turns’
Episodes of transient disturbance of consciousness are common clinical problems (Table 17.3). Differentiation of seizures from other disorders often depends entirely on the medical history. An eye-witness account is
Table 17.1 Causes of headache |
Acute severe (onset in minutes or hours) Intracranial haemorrhage Cerebral venous thrombosis Dissection of carotid/vertebrobasilar arteries Meningitis Head injury Migraine Drugs, e.g. glyceryl trinitrate Alcohol Infections, e.g. malaria Subacute onset (onset in days to weeks) Intracranial mass lesion Encephalitis Meningitis Giant cell arteritis Sinusitis Acute glaucoma Malignant hypertension Recurrent/chronic Migraine Tension headache Sinusitis Cluster headaches Paroxysmal hemicrania Medication overuse Intracranial mass lesion |
Table 17.2 Indications for brain imaging in patients with headache |
Sudden onset New headache in a patient over 50 years of age Abnormal neurological signs Headache changing with posture (may indicate raised ICP) Headache made worse by coughing, sneezing, bending, straining (may indicate raised ICP) Fever History of HIV History of cancer ICP, intracranial pressure |
Table 17.3 Common causes of attacks of altered consciousness and falls in adults |
Syncope – cardiopulmonary causes Underlying structural cardiopulmonary disease, e.g. aortic stenosis, PE Arrhythmias Syncope – vascular causes Reflex: vasovagal (simple faint) Carotid sinus hypersensitivity Situational: cough, micturition, postexertional Postural (orthostatic) hypotension: autonomic failure, volume depletion Epilepsy Hypoglycaemia Psychogenic Panic attacks Hyperventilation Narcolepsy and cataplexy PE, pulmonary embolism |
invaluable. Differentiation must also be made from narcolepsy, a rare disorder characterized by periods of irresistible sleep in inappropriate circumstances and cataplexy, a related condition in which sudden loss of tone develops in the lower limbs, with preservation of consciousness. Attacks are set off by sudden surprise or emotion.
Dizziness and syncope
Syncope describes a short duration (usually 20-30 seconds) of loss of con-sciousness caused by a global reduction in cerebral blood flow. There is usually a rapid and complete recovery. Syncope is a symptom rather than a disease. It can be caused by several underlying conditions (Table 17.3) and is often mistaken for epilepsy.
Dizziness or faintness precedes syncope, and represents an incomplete form in which cerebral perfusion has not fallen sufficiently to cause loss of consciousness. Dizziness should be differentiated from vertigo (p. 704), which is an illusion of rotary movement where the patient feels that the sur-roundings are spinning. It results from disease of the inner ear, the eighth cranial nerve, or its central connections.
The most frequent cause of dizziness is vasovagal syncope (a simple faint), which occurs as a result of reflex bradycardia and peripheral and splanchnic vasodilatation. Fear, pain and prolonged standing are the principal causes. Fainting almost never occurs in the recumbent position. A prodrome of nausea, pallor, lightheadedness and sweating usually precede a faint. Rapid recovery from the attack and the absence of jerking movements suggest a faint as opposed to a fit. Urinary incontinence may occur during syncope.
Loss of consciousness due to an arrhythmia occurs without warning and may occur in the supine position. Syncope may occur after micturition in men (particularly at night), and when the venous return to the heart is obstructed by breath-holding and severe coughing. Effort syncope occurs on exercise and occurs in patients with aortic stenosis and hypertrophic cardiomyopathy. Carotid sinus syncope is thought to be the result of excessive sensitivity of the sinus to external pressure. It occurs in elderly patients who lose con-sciousness following pressure on the sinus (e.g. turning the head). Postural hypotension (drop in systolic BP >20 mm Hg from lying to standing position after 3 minutes) occurs on standing in those with impaired autonomic reflexes, e.g. elderly people, in autonomic neuropathy and with some drugs (phenothiazines, tricyclic anti-depressants).
Investigation
The history and physical examination together with lying and standing blood pressure and a 12 lead ECG will provide a diagnosis in most people with transient loss of consciousness. Echocardiography is used to determine any underlying structural heart disease. Ambulatory electrography (p. 415) has a low diagnostic yield unless symptoms are frequent. Tilt table testing (p. 417) is performed to investigate patients with unexplained syncope in whom cardiac causes or epilepsy have been excluded. Blood pressure, heart rate, symptoms and ECG are recorded after head-up tilt for 10-60 minutes. Repro-duction of symptoms and hypotension indicate a positive test.
Weakness
Skeletal muscle contraction is controlled by the motor axis of the central nervous system (Fig 17.1). Muscle weakness occurs due to a defect or damage in one or more components of this system, i.e. the motor cortex, corticospinal tracts, anterior horn cells, spinal nerve roots, peripheral nerves, the neuro-muscular junction and muscle fibres. It is necessary to determine whether there is true weakness rather than ‘tiredness' or ‘slowness', as in Parkinson's disease. The site of the lesion causing true muscle weakness is often identifiable from a detailed neurological examination. The distribution of weakness, the presence or absence of deep tendon reflexes, the plantar response (Table 17.4) and related sensory defects are all helpful in localizing the lesion in the nervous system. Lesions that affect the upper motor neurone and peripheral nerve will also often involve the sensory system because of the proximity of sensory to motor nerves in these areas.
The corticospinal tracts
The upper motor neurone The corticospinal tracts originate from neurones of the motor cortex and terminate on the motor nuclei of the cranial nerves and the anterior spinal horn cells. The pathways cross over in the medulla and pass to the contralateral halves of the spinal cord as the crossed lateral
Fig. 17.1 The crossed corticospinal (‘pyramidal') tracts showing cortical representation of various parts of the body.
Table 17.4 Comparison of the clinical features of upper and lower motor neurone lesions |
|
Upper motor neurone lesion* |
Lower motor neurone lesion |
Signs are on the opposite side to the lesion |
Signs are on the same side as the lesion |
Fasciculation absent |
Fasciculation present |
No muscle wasting |
Wasting |
Spasticity ± clonus |
Hypotonia |
Weakness predominantly extensors in the arms, flexors in the legs |
|
Exaggerated tendon reflexes |
Loss of tendon reflexes |
Extensor plantar response | |
Drift of the outstretched hand |
|
(downwards, medially with a tendency to pronate) |
|
Fasciculation = visible contraction of single motor units, appearing as a twitch *Acute injury to the UMN is, however, manifest by transient flaccid weakness and hyporeflexia |
corticospinal tracts (Fig. 17.1), which then synapse with the anterior horn cells. This is known as the pyramidal system, disease of which results in upper motor neurone (UMN) lesions with characteristic clinical features (Table 17.4). Appropriate imaging studies of the central nervous system and spine such as MRI or CT scan will be necessary to identify the primary disease.
Two main patterns of clinical features occur in UMN disorders: hemi-paresis and paraparesis:
■ Hemiparesis means weakness of the limbs of one side, and is usually caused by a lesion within the brain or brainstem, e.g. a stroke.
■ Paraparesis (weak legs) indicates bilateral damage to the corticospinal tracts and is most often caused by lesions in the spinal cord below T1 (p. 779). Tetraparesis (quadriplegic, weakness of the arms and legs) indicates high cervical cord damage, most commonly resulting from trauma. Cord lesions result in UMN signs below the lesion, LMN signs at the level of the lesion and unaffected muscles above the lesion.
The lower motor neurone The lower motor neurone (LMN) is the motor pathway from the anterior horn cell or cranial nerve via a peripheral nerve to the motor endplate. Physical signs (Table 17.4) follow rapidly if the LMN is interrupted at any point in its course. Muscle disease may give a similar clinical picture, but reflexes are usually preserved.
LMN lesions are most commonly caused by the following:
■ Anterior horn cell lesions, e.g. motor neurone disease, poliomyelitis
■ Spinal root lesions, e.g. cervical and lumbar disc lesions
■ Peripheral nerve lesions, e.g. trauma, compression or polyneuropathy. The commonest disease of the neuromuscular junction is myasthenia gravis, which characteristically produces weakness of skeletal muscle and is rarely associated with wasting. Myopathies are discussed on page 790. Weakness of the proximal muscles, e.g. quadriceps, is typically seen with the various myopathies. Elevation of plasma muscle enzymes such as creatine kinase is highly suggestive of muscle diseases. Muscle biopsy may be necessary to determine the precise form of myopathy.
Numbness
The sensory system
The peripheral nerves carry all the modalities of sensation from nerve endings to the dorsal root ganglia and thence to the cord. These then ascend to the thalamus and cerebral cortex in two principal pathways (Fig. 17.2):
■ Posterior columns, which carry sensory modalities for vibration, joint position sense (proprioception), two-point discrimination and light touch. These fibres ascend uncrossed to the gracile and cuneate nuclei in the medulla. Axons from the second-order neurones cross the midline to form the medial lemniscus and pass to the thalamus.
■ Spinothalamic tracts, which carry sensations of pain and temperature. These fibres synapse in the dorsal horn of the cord, cross the midline and ascend as the spinothalamic tracts to the thalamus.
Paraesthesiae (pins and needles), numbness and pain are the principal symptoms of lesions of the sensory pathways below the level of the thalamus. The quality and distribution of the symptoms may suggest the site of the lesion.
Peripheral nerve lesions Symptoms are felt in the distribution of the affected peripheral nerve, e.g. the ulnar or median nerve. Polyneuropathy is a subset of the peripheral nerve disorders characterized by bilateral sym-metrical, distal sensory loss and burning (p. 787).
Spinal root lesions Symptoms are referred to the dermatome supplied by that root, often with a tingling discomfort in that dermatome (Fig. 17.3). This is in contrast to lesions of sensory tracts within the central nervous system, which characteristically present as general defects in an extremity rather than specific dermatome defects.
Spinal cord lesions Symptoms (e.g. loss of sensation) are usually evident below the level of the lesion. A lesion of the pain-temperature pathway (spinothalamic tract), whether within the brainstem or the spinal cord, will result in loss of pain-temperature sensation contralaterally, below the level
Fig. 17.2 A schematic outline of the major motor and sensory pathways
Fig. 17.3 Simple scheme depicting motor and sensory innervation of arms and legs and root values for reflexes. (Part of figure adapted from Parsons M (1993) A Colour Atlas of Clinical Neurology. London, Mosby Wolfe.)
of the lesion. A lesion at the spinal level of the pathway for proprioception will result in loss of these senses ipsilaterally below the level of the lesion. Dissociated sensory loss suggests a spinal cord lesion, for instance loss of pain-temperature sensation in the right leg and loss of proprioception in the left leg.
Pontine lesions The pons lies above the decussation of the posterior columns. As the medial lemniscus and spinothalamic tracts are close together, pontine lesions result in the loss of all forms of sensation on the side opposite the lesion.
Thalamic lesions A thalamic lesion is a rare cause of complete contra-lateral sensory loss. Spontaneous pain may also occur, most commonly as the result of a thalamic infarct.
Cortical lesions Sensory loss, neglect of one side of the body and subtle disorders of sensation may occur with lesions of the parietal cortex. Pain is not a feature of cortical lesions.
Tremor
Tremor is a rhythmic involuntary muscular contraction characterized by oscillations of a part of the body. A resting tremor is seen in Parkinson's disease, parkinsonism and Wilson's disease. Postural tremor occurs when a patient attempts to maintain a posture such as holding the arms out-stretched. Causes include physiological (due to any increase in sympathetic activity), essential tremor (p. 761), and in some cases of Parkinson's disease and cerebellar disease. Intention tremor occurs during voluntary movement and gets worse when approaching the target, e.g. during finger to nose testing, and occurs with cerebellar disease. Task specific tremor appears when performing goal-orientated tasks such as handwriting, speaking or standing. In many cases the cause of a tremor will be apparent from the history and examination. Investigations include thyroid function tests, testing for Wilson's disease (in anyone under 40 years) and brain imaging in selected cases.
1. Ethics and communication
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3. Gastroenterology and nutrition
Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
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Malignant disease
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18. Dermatology