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Neurologic Complications Of Other Infections
The classification of the parainfectious encephalopathies has been clarified by Ropper, who suggests four categories of disorder:
Encephalitis caused by direct viral invasion of the brain
Acute toxic encephalopathy, with brain swelling rather than inflammation
Postinfectious or postvaccinal encephalopathy (also called acute disseminated or acute allergic encephalomyelitis) is a multifocal demyelinating disease with an immunologic basis
An inflammatory encephalitis occurs with Epstein-Barr virus, influenza, and mycoplasma infections that cannot be clinically distinguished from ordinary viral encephalitis, but the agent is not recoverable from the brain
The findings in encephalitis have already been discussed; we will describe the encephalopathies named above under the older, popular headings.
Fever and acute neurologic signs may suddenly appear during or within 2 weeks of acute specific (e.g., measles) or nonspecific infections in children, during the acute illness in bacterial endocarditis in adults, or after vaccination in anyone. Typical signs include meningism, acute obtundation and delirium, seizures, myoclonus, cerebellar signs, chorea, and evidence of raised ICP. The CSF is usually normal. A few patients recover completely but most are left with significant residual neurologic deficits or epilepsy. No infective agent has ever been isolated from the brain in these cases, and the etiology is presumed to be an allergic vasculitis.
Reye's syndrome is a form of acute toxic encephalopathy that occurs in children and young adults, possibly as a complication of a preceding influenza or varicella infection, or use of acetylsalicylic acid (ASA) in children. Encephalopathy (delirium, seizures, coma, and inconstant focal signs) follows a period of malaise and fever with persistent vomiting. Fatty degeneration of the liver and cerebral edema with a marked rise in ICP are the pathologic basis of these signs. Because intensive metabolic therapy may be lifesaving, immediate referral is essential whenever even drowsiness follows prolonged vomiting in young people.
Alternative names for acute postinfectious encephalomyelitis are allergic or postvaccinal encephalomyelitis. These are a group of similar disorders characterized by a monophasic course after a febrile illness or vaccination. Multiple perivenular foci of demyelination and lymphocytic infiltration appear in the nervous system with secondary damage to axons. Thus, unlike the acute encephalitides, the white rather than the grey matter is primarily affected.
Characteristically, this disorder occurs 1 to 2 weeks after an acute infection or an immunologic challenge. The presumed pathogenesis is an autoimmune reaction to brain myelin, after either vaccination (e.g., against rabies or smallpox) or infection with measles, rubella, chickenpox,
The incubation period is 8 to 15 days, after which there is an abrupt onset of headache, with signs of raised ICP and drowsiness that may progress to coma. Before coma develops, the patient may have nausea, vomiting, high fever, meningism, myoclonus or seizures, flaccid paralysis, and variable sensory loss. Cerebellar ataxia is sometimes the main feature. The brunt of the disease may be borne by the brain, the spinal cord, or occasionally by the spinal nerve roots (producing a radiculopathy). The CSF is under increased pressure and contains excess protein and sometimes increased mononuclear cells, but no virus is isolated.
Steroids in high dosage in the early stages of this disease are probably effective in reducing the immunologic reaction, and concern about spreading a viral infection is probably unjustified. At the other end of the scale, the clinical picture may be identical with that of epidemic myalgic encephalomyelitis, and illnesses of any intermediate stage of severity are also possible. Despite therapy, a majority of the patients will either die or be left with serious neurologic deficits. Others recover, often with some neurologic sequelae.
The distinction from multiple sclerosis is made by the presence of fever, the monophasic character of the illness without any past history of neurologic symptoms, a painful radiculopathy in many cases, and the flaccid paresis. The EEG shows bilateral delta activity in a high proportion of patients but is not diagnostic, although such recordings are not commonly seen in multiple sclerosis.
Over one third of the patients with bacterial endocarditis present with neurologic signs. Half of these appear to have cerebrovascular disease (usually an infarct, but occasionally a hemorrhage). In the later stages, mycotic aneurysms may rupture and cause a subarachnoid hemorrhage. Acute toxic encephalopathy with delirium can occur, and some patients have a clinical presentation indistinguishable from acute meningitis or cerebral abscess. In these cases the CSF usually contains mononuclear cells but no organisms, although S. aureus is the most common infecting agent. Other complications of bacterial endocarditis include retinal hemorrhages, seizures, and recurring headaches (
Children with bacterial endocarditis often show a rash in association with fever and delirium, and this picture must be differentiated from that caused by the acute specific fevers such as scarlet fever, measles, enterovirus and adenovirus infections, and rubella and by allergic and drug reactions. Purpura with fever may occur in mononucleosis, rickettsial disease, Henoch-Schönlein purpura, and in other types of allergic vasculitis.
Cerebral abscesses in association with sinus infection or otitis usually occur as a result of direct extension of the infection within or alongside the dural sinuses and the other large intracranial veins. Sometimes the brain is not directly involved itself, but the infection in the walls of the veins causes venous thrombosis with venous infarction of the portions of the brain drained by the occluded vessels. In children, sinus thrombosis can occur without local infection at all, as in marked dehydration or high fevers. Sinus thrombosis may also complicate sickle cell anemia and severe cachexia, in which case the superior sagittal sinus is usually involved. It may also occur in women in the postpartum period or those who are taking oral contraceptives. An association with polycythemia and with lymphomas has also been recognized.
Clinical features include those of local ear or sinus infection complicated by seizures, raised ICP caused by failure of venous drainage, meningism, and sometimes focal neurologic findings as a result of venous infarction. Otitis usually produces thrombophlebitis in the transverse sinuses, and there may be little in the way of focal signs. General examination may show evidence of systemic disorders such as those listed in
Sinus thrombosis complicating mastoiditis may also present subacutely with raised ICP without meningism, a condition described as otitic hydrocephalus. Cavernous sinus thrombosis (
Distinction between sinus thrombophlebitis and cerebral abscess or meningitis may be difficult, although brain scanning and EEG will probably not show the clear-cut localizing features to be expected with cerebral abscesses. The diagnosis is probably best made by MRI and carotid arteriography. The CSF pressure, lymphocyte count, and protein level are high. Red cells may be present with thrombophlebitis, but organisms are not detected and are only cultured from the blood.
If cerebral abscess seems clinically likely, however, LP is best deferred until the patient is in a neurologic center, because it is dangerous and often is unnecessary when a CT scanner is available.
Treatment consists of attempts to lower the ICP with steroids or dehydrating solutions and the use of high doses of broad-spectrum antibiotics. Ligation of the infected veins is of questionable value. Where specific underlying medical disease is found, this may be treatable. Anticoagulants are of doubtful value in sinus thrombosis.
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Textbook of Primary Care Medicine, 3rd ed
By: T. Jock Murray, William Pryse-Phillips © 2005 ELSEVIER Inc. All Rights Reserved |
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