COMMON NEUROLOGICAL SYMPTOMS

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.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology



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