NERVOUS SYSTEM INFECTION AND INFLAMMATION

Meningitisnd

Meningitis (inflammation of the meninges) can be caused by infection, intrathecal drug, malignant cells and blood (following subarachnoid haemor-rhage). The term is, however, usually reserved for inflammation caused by infective agents (Table 17.14). Microorganisms reach the meninges either by direct extension from the ears, nasopharynx, cranial injury or congenital meningeal defect, or by bloodstream spread. Immunocompromised patients (HIV, cytotoxic drug therapy) are at risk of infection by unusual organisms.

Clinical features

Acute bacterial meningitis Headache, neck stiffness and fever develop over minutes to hours. Photophobia (intolerance of light) and vomiting are often present. Kernig's sign (inability to allow full extension of the knee when the hip is flexed 90°) is usually present. Consciousness is usually not

Table 17.14 Infective causes of meningitis in the UK
Bacteria
Neisseria meningitidis*
Streptococcus pneumoniae*
Staphylococcus aureus
Streptococcus group B
Listeria monocytogenes
Gram-negative bacilli, e.g. E. coli
Mycobacterium tuberculosis†
Treponema pallidum†
Viruses
Enterovirus (ECHO, Coxsackie)
Poliomyelitis
Mumps
Herpes simplex virus
HIV
Epstein–Barr virus
Fungi†
Cryptococcus neoformans
Candida albicans
Coccidioides immitis
Histoplasma capsulatum
*account for most cases of acute bacterial meningitis outside of the neonatal period.
†may cause chronic meningitis with signs and symptoms for longer than 4 weeks.

impaired, although the patient may be delirious with a high fever. Papil-loedema may occur. Progressive drowsiness, lateralizing signs and cranial nerve lesions indicates the existence of a complication, e.g. venous sinus thrombosis, severe cerebral oedema or cerebral abscess. In meningococcal septicaemia there is a non-blanching petechial and purpuric skin rash and signs of shock.

Viral meningitis is usually a benign self-limiting condition lasting for about 4-10 days. There are no serious sequelae.

Chronic meningitis presents with a long history and vague symptoms of headache, lassitude, anorexia and vomiting. Signs of meningism may be absent or appear late in the course of the disease.

Differential diagnosis

Subarachnoid haemorrhage, migraine, viral encephalitis and cerebral malaria can mimic meningitis.

Management

Suspected bacterial meningitis is a medical emergency with a high mortality rate and requires urgent investigation and treatment (Emergency Box 17.3).

Notification

All cases of meningitis must (by law in the UK) be notified to the local Public Health Authority; this allows contact tracing and provides data for epidemio-logical studies.

Emergency Box 17.3

Investigation and treatment of suspected bacterial meningitis
Note: A non-blanching petechial or purpuric skin rash is indicative of meningococcal infection. It is an indication for immediate (before hospital transfer) treatment with benzylpenicillin, 1200 mg by slow i.v. or i.m. injection or cefotaxime 1 g i.v. Lumbar puncture should not be performed if meningococcal sepsis is suspected because coning of the cerebellar
tonsils may follow – the organism is confirmed by blood culture.
Investigations
• Head CT scan should be performed if there is any suspicion of an intracranial mass lesion such as focal neurological signs, papilloedema, loss of consciousness or seizure.
• Lumbar puncture (LP). Urgent CSF microscopy, white cell count and differential, and analysis for protein and glucose concentration (Table 17.15). Auramine stain (tuberculous) and Indian ink stain (cryptococcal infection) in immunocompromised or other at-risk individual.
• Other. Blood cultures, blood glucose, chest X-ray, viral and syphilis serology.
Treatment
Note: Antimicrobial therapy should not be delayed if there is a contraindication or inability to perform immediate LP.
• Close liaison between clinician and microbiologist is essential
• Cefotaxime 2 g 6-hourly i.v. for the initial treatment of bacterial meningitis. Add ampicillin 2 g 4-hourly or co-trimoxazole if risk of Listeria (elderly, immunosuppressed)
• Subsequent treatment given depending on results of Gram stain and culture, and antibiotic sensitivities of the organism
• Intravenous fluids and inotropes are given if there is also septicaemia (p. 577)
• Tuberculous meningitis is treated for at least 9 months (p. 544)

Table 17.15 Typical changes in the CSF in viral, bacterial and TB meningitis

Normal

Bacterial

Viral

Tuberculous

Appearance

Clear

Turbid/purulent

Clear/turbid

Turbid/viscous

Mononuclear cells/mm3

<5

<50

10-100

100-300

Polymorphs/mm3

Nil

200-3000

Nil

0-200

Protein (g/L)

0.2-0.4

0.5-2.0

0.4-0.8

0.5-3.0

Glucose (% blood glucose)

>50

<50

>50

<50

NB: Malignant meningitis, e.g. with lymphoma, may give similar changes to TB

Meningococcal prophylaxis

Oral rifampicin or ciprofloxacin is given to eradicate nasopharyngeal carriage of the organism. It is given to patients and those who have had prolonged close contact in a household setting during the 7 days before onset of the illness. A vaccine for meningococcal group C and Haemophilus influenzae is part of routine childhood UK immunization.

Encephalitis

Encephalitis is inflammation of the brain parenchyma. Unlike meningitis, cerebral function is usually abnormal with altered mental status, motor and sensory deficits. It is caused by a wide variety of viruses and may also occur in bacterial and other infections. In certain groups (e.g. men who have sex with men, intravenous drug users), HIV infection and opportunistic organisms (e.g. Toxoplasma gondii in patients with full-blown AIDS) are causes.

Acute viral encephalitis

A viral aetiology is often presumed, although not confirmed serologically or by culture. In the UK the common organisms are herpes simplex viruses, ECHO, Coxsackie and mumps. Epidemic and endemic viral encephalitides occur world-wide, e.g. Japanese encephalitis (arbovirus) in South-East Asia, West Nile encephalitis in Egypt and Sudan. Tick-borne encephalitis (TBE) is caused by the TBE virus, a member of the Flaviviridae, and exists in two major forms: Central European and Far Eastern. An inactivated vaccine is available for travellers spending time in endemic areas.

Clinical features

Many of these infections cause a mild self-limiting illness with fever, head-ache and drowsiness. Less commonly the illness is severe, with focal signs (e.g. hemiparesis, dysphasia), seizures and coma. Death or brain injury follows; herpes simplex virus (HSV-1) accounts for many of these in the UK.

Investigations

■ CT and MR imaging shows areas of oedema often in the temporal lobes

■ CSF analysis shows a moderate increase in mononuclear cells (5-500 cells/mm3). Protein may also be increased

■ Viral serology of blood and CSF may identify the causative virus

■ EEG often shows non-specific slow-wave activity.

Treatment

Suspected herpes simplex encephalitis is immediately treated with intra-venous aciclovir (10 mg/kg every 8 hours for 14-21 days). If the patient is in a coma the prognosis is poor, whether or not treatment is given.

Brain and spinal abscesses

An intracranial abscess may develop in the epidural, subdural or intra-cerebral sites. Epidural abscesses are uncommon; subdural abscess presents similarly to intracerebral abscess.

Cerebral abscess

Infection follows the direct spread of organisms from a parameningeal infec-tive focus (e.g. paranasal sinuses, middle ear or skull fracture) or a distant source of infection via the bloodstream (lung, heart, abdomen). Frequently no cause is found. The most common organisms are Streptococci anginosus, Bacteroides species and staphylococci. Infection with tubercle bacilli may result in chronic caseating granulomata (tuberculomas) presenting as intra-cranial mass lesions.

Clinical features

These include headache, focal neurological signs, seizures and sometimes evidence of raised intracranial pressure (p. 772) developing over days to weeks. Fever is usual but not invariable.

Investigations

Contrast enhanced CT scan will show the abscess. Lumbar puncture is not performed because of the danger of coning in the presence of raised intracranial pressure (p. 737). Aspiration with stereotactic guidance allows the organism to be identified.

Management

Treatment is with a combination of intravenous antibiotics and sometimes surgical decompression.

Spinal epidural abscess

Back pain and fever are followed by paraparesis and/or root lesions. The abscess is shown on MR imaging and treatment is with antibiotics (organism is usually Staphylococcus aureus) and surgical decompression.

Neurosyphilis

Syphilis is described on page 43. Neurosyphilis occurs late in the course of untreated infection and is now rarely seen in the UK because of treatment at an earlier stage. The different clinical syndromes (Table 17.16) occur alone or in combination.

Table 17.16 The clinical syndromes of neurosyphilis

Asymptomatic neurosyphilis

Positive CSF serology without symptoms or signs

Meningovascular syphilis (3-4 years)

Subacute meningitis with cranial nerve palsies and papilloedema
Gumma (an expanding intracranial mass) causes raised intracranial pressure and focal deficits
Paraparesis caused by spinal meningovasculitis

General paralysis of the insane (10-15 years)

Progressive dementia
Brisk reflexes
Extensor plantar responses
Tremor

Tabes dorsalis (10-35 years)

Demyelination in the dorsal roots causes lightning pains (short, sharp, stabbing) in the legs Ataxia, loss of reflexes and sensory loss Neuropathic joints (Charcot’s joints)
Argyll Robertson pupils (p. 730), ptosis and optic atrophy

The numbers in brackets are the years after the primaiy infection.

Management

Treatment is with benzylpenicillin 1 g daily i.m. for 10 days, which may arrest (but not reverse) the neurological disease.

Transmissible spongiform encephalopathy (Creutzfeldt-Jakob disease (CJD))

There is progressive dementia, usually developing after 50 years of age, characterized pathologically by spongiform changes in the brain. It is caused by prions (a proteinaceous infectious particle) and the pathology is similar to bovine spongiform encephalopathy (BSE) of cattle. Prions are resistant to many of the usual processes that destroy proteins. CJD occurs as a sporadic form or an iatrogenic form as a result of contaminated material such as corneal grafts or human growth hormone. There is no treatment and death usually occurs within 6 months of onset.

Variant CJD (vCJD) presents with neuropsychiatric symptoms, followed by ataxia and dementia, and affects a younger age group. Diagnosis can be confirmed by tonsillar biopsy and CSF gel electrophoresis. vCJD and BSE are caused by the same prion strain suggesting transmission from BSE-infected cattle to the human food chain.

BRAIN TUMOURS

Primary intracranial tumours account for 10% of all neoplasms, and in the UK about half of all intracranial tumours are metastatic. Primary intracranial tumours are derived from the skull itself, or from any of the structures lying within it, or from their tissue precursors. They may be malignant on histologi-cal investigation but rarely metastasize outside the brain. The most common intracranial tumours occurring in adults are listed in Table 17.17. Pituitary tumours are discussed separately on page 611.

Clinical features

The clinical features of a cerebral tumour are the result of the following:

■ Progressive focal neurological deficit

■ Raised intracranial pressure

■ Focal or generalized epilepsy.

Neurological deticit is the result of a mass effect of the tumour and surrounding cerebral oedema. The deficit depends on the site of the tumour, e.g. a frontal lobe tumour will initially cause personality change, apathy and intellectual deterioration. Subsequent involvement of the frontal speech area and motor cortex produces expressive aphasia and hemiparesis. Rapidly growing tumours destroy cerebral tissue and loss of function is an early feature.

Table 17.17 Common brain tumours  
Tumour Relative frequency (%)
Primary malignant 35
Glioma  
Embryonal tumours, e.g. medulloblastoma  
Lymphoma  
Benign 15
Meningioma  
Neurofibroma  
Metastases 50
Bronchus
 
Breast  
Stomach  
Prostate  
Thyroid  
Kidney  
Gliomas, meningiomas and embryonal tumours account for 95% of primary brain tumours

Ralsed intracranial pressure produces headache, vomiting and papil-loedema. The headache typically changes with posture and is made worse by coughing, sneezing, bending and straining.

As the tumour grows there is downward displacement of the brain and pressure on the brainstem, causing drowsiness, which progresses eventually to respiratory depression, bradycardia, coma and death. Distortion of normal structures at a distance from the growing tumour leads to focal neurological signs (false localizing signs). The most common are a third and sixth cranial nerve palsy (p. 731) resulting from stretching of the nerves by downward displacement of the temporal lobes.

Epllepsy Fits may be generalized or partial in nature. The site of origin of a partial seizure is frequently of value in localization.

Differential diagnosis

The main differential is from other intracranial mass lesions (cerebral abscess, tuberculoma, subdural haematoma and intracranial haematoma) and a stroke, which may have an identical clinical presentation. Benign (idio-pathic) intracranial hypertension presents with headache and papilloedema in young obese females. Neuroimaging is normal but at lumbar puncture there is raised CSF pressure.

Investigations

■ Imaging. CT and MRI are useful in detecting brain tumours. MRI is of particular value in investigation of tumours of the posterior fossa and brainstem. MR angiography is sometimes necessary to define the site or blood supply of a mass, particularly if surgery is planned. Positron emis-sion tomography (PET) is sometimes helpful to locate an occult primary tumour with metastasis. Plain skull X-rays have no value in brain tumour diagnosis.

■ Other investigations. These include routine tests, e.g. chest X-ray if metastatic disease is suspected. Lumbar puncture and examination of the CSF is contraindicated with the possibility of an intracranial mass lesion because of danger of immediate herniation of the cerebellar tonsils, impaction within the foramen magnum and compression of the brainstem (‘coning').

Management

■ Surgery. Surgical exploration, and either biopsy or removal of the mass, is usually carried out to ascertain its nature. Some benign tumours, e.g. meningiomas, can be removed in their entirety without unacceptable damage to surrounding structures.

■ Radiotherapy is given for gliomas and radiosensitive metastases and improves survival slightly.

■ Medical treatment. Cerebral oedema surrounding a tumour is rapidly reduced by corticosteroids; i.v. or oral dexamethasone. Epilepsy is treated with anti-convulsants. Chemotherapy has little real value in the majority of primary or secondary brain tumours. The prognosis is very poor in patients with malignant tumours, with only 50% survival at 2 years for high-grade gliomas.

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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