SPINAL CORD DISEASE

The cord extends from C1 (its junction with the medulla) to the vertebral body of L1. The spinal canal below L1 is occupied by lumbar and sacral nerve roots, which group together to form the cauda equina and ultimately extend into the pelvis and thigh (Fig. 17.11). Paraplegia (weakness of both legs) is almost always caused by a spinal cord lesion, as opposed to hemiplegia (weakness of one side of the body), which is usually the result of a lesion in the brain.

Fig. 17.11 The spinal cord and cauda equina. The bony vertebrae are indicated on the left-hand side (7 cervical, 12 thoracic, 5 lumbar and 5 sacral). The spinal cord extends from C1 (its junction with the medulla) to the vertebral body of L1. The spinal cord segments indicated on the right are not necessarily situated at the same vertebral levels as the bony vertebra. For instance the lumbar cord is situated between T9 and T11 vertebrae. A T8 vertebral injury will result in a T12 cord or neurological level (i.e. sensation is diminished below the T12 dermatome, and motor function is reduced in muscles innervated by T12 and below). The cord segmental levels are indicated for cervical (blue), thoracic (red), lumbar (green) and sacral (yellow). The spray of spinal roots below the conus is called the cauda equina and is damaged by lesions below the L2 vertebra.

Spinal cord compression

This is a medical emergency.

Clinical features

There is progressive weakness of the legs with upper motor neurone pattern (Table 17.4) and eventual paralysis. The onset may be acute (hours to days) or chronic (weeks to months), depending on the cause. The arms are affected if the lesion is above the thoracic spine. There is sensory loss below the level of the lesion. This is called the sensory level and is when sensation abruptly diminishes one to two spinal cord segments below the level of the actual anatomical level of spinal cord compression. Sometimes there is loss of sphincter control with urinary incontinence. There may be painless urinary retention and constipation in the later stages.

Aetiology

The most common cause of acute spinal cord compression is a vertebral tumour (metastases from lung, breast, kidney, prostate or multiple myeloma (Table 17.18)). Spinal tuberculosis is a frequent cause in endemic areas (p. 541).

Investigations

Urgent investigation is essential in a patient with suspected cord compres-sion, especially with acute or subacute onset, because irreversible paraplegia may follow if the cord is not decompressed.

Table 17.18 Causes of spinal cord compression

Vertebral body neoplasms

Metastases, e.g. from lung, breast, prostate

Myeloma

Lymphoma

Disc and vertebral lesions

Trauma

Chronic degenerative disease

Inflammatory

Epidural abscess

Tuberculosis (Pott’s paraplegia)

Spinal cord neoplasms

Primary cord neoplasm, e.g. glioma, neuroíibroma

Metastases

Rarities

Paget’s disease, bone cysts, osteoporotic vertebral collapse

  Epidural haemorrhage, e.g. patients on warfarin

■ MRI identifies the cause and site of cord compression

■ X-ray of the spine may show degenerative bone disease and destruction of vertebrae by infection or neoplasm.

Management

The treatment depends on the cause, but in most cases the initial treatment involves surgical decompression of the cord and stabilization of the spine. Dexamethasone (16 mg/day, p. 663) reduces oedema around the lesion and improves outcome in patients with cord compression due to malignancy.

Differential diagnosis

The differential diagnosis is from intrinsic lesions of the cord causing para-paresis. Transverse myelitis (acute inflammation of the cord resulting from viral infection, syphilis or radiation therapy), anterior spinal artery occlusion and multiple sclerosis may present with a rapid onset of paraparesis. A more insidious onset of weakness occurs with motor neurone disease (in which there is no sensory deficit), subacute combined degeneration of the cord, and as a non-metastatic manifestation of malignancy. MRI should always be performed in a patient with a sensory or motor level. Rarely a parasagittal cortical lesion, e.g. meningioma, may cause paraplegia.

Cauda equina lesion

Spinal damage at or distal to L1 (a common cause is lumbar disc prolapse at the L4/L5 and L5/S1 level) injures the cauda equina (p. 778). Cauda equina syndrome can present acutely or with a more insidious onset of typical signs and symptoms. Involvement of multiple sacral and lumbar nerve roots in the lumbar vertebral canal causes bladder (reduced desire to void progressing to painless urinary retention), and bowel dysfunction and perianal and perineal ('saddle') numbness. There may also be back pain, numbness and weakness in the legs with reduced reflexes. MRI is the imaging method of choice in patients with suspected cauda equina syndrome and surgical decompression if a potentially revesible cause is shown.

Syringomyelia and syringobulbia

Fluid-filled cavities within the spinal cord (myelia) and brainstem (bulbia) are the essential features of these conditions.

Aetiology

The most frequent cause is blockage of CSF flow from the fourth ventricle in association with an Arnold-Chiari malformation (congenital herniation of the cerebellar tonsils through the foramen magnum). The normal pulsatile CSF pressure waves are transmitted to the delicate tissues of the cervical cord and brainstem, with secondary cavity formation. Hydrocephalus may also occur as a result of disturbed CSF flow.

Clinical features

Patients usually present in the third or fourth decade with pain and sensory loss (pain and temperature) in the upper limbs. The clinical features are demonstrated in Figure 17.12.

Investigation

MRI is the investigation of choice and demonstrates the intrinsic cavities.

Fig. 17.12 Production of physical signs in syringomyelia. Expanding cavities distend the cord. Pain and temperature (A) fibres crossing at that level are destroyed, but sensory fibres in the posterior columns (other sensory modalities) and those that enter the spinothalamic tract at a lower level are spared. Sensory loss is therefore ‘dissociated’ and confined to the upper trunk and limbs. Further extension damages the anterior horn cells (B), the pyramidal tracts (C) and the medulla, causing wasting in the hands, a spastic paraplegia, nystagmus and a bulbar palsy. (From Parsons M (1993) A Colour Atlas of Clinical Neurology. London Mosby Wolfe.)

Treatment

Surgical decompression of the foramen magnum sometimes slows deterioration.

Friedreich’s ataxia

This autosomal recessive disorder is the most common of the hereditary spinocerebellar degenerations. There is a progressive degeneration of the spinocerebellar tracts and cerebellum causing cerebellar ataxia, dysarthria and nystagmus. Degeneration of the corticospinal tracts causes weakness and an extensor plantar response. The tendon reflexes are absent as a result of peripheral nerve damage. Loss of the dorsal columns causes absent joint position and vibration sense. Other features are pes cavus, optic atrophy, cardiomyopathy, and death by middle age.

Management of the paraplegic patient

The paraplegic patient requires skilled and prolonged nursing care. A pressure-relieving mattress and turning the patient every 2 hours helps to prevent pressure sores. Bladder catheterization (sometimes intermittent self-catheterization) prevents urinary stasis and infection. Patients may need manual evacuation of faeces. This may become unnecessary as reflex empty-ing of the bladder and rectum develops. Passive physiotherapy helps to prevent contractures in paralysed limbs. Severe spasticity may be helped by dantrolene sodium, baclofen or diazepam. Many patients graduate to a wheelchair and maintain some degree of independence.

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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