Neurologic Complications

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Central nervous system (CNS) disease occurs in 90 percent of patients with AIDS, and 10 to 20 percent of HIV-infected patients initially present with CNS symptoms.17 Neurologic disease is caused by a variety of opportunistic infections and neoplasms as well as the direct and indirect effects of HIV infection on the CNS. Common presenting symptoms indicative of CNS pathology include seizures, altered mental status, headache, meningismus, and focal neurologic deficits. 17 Emergency department evaluation should include a complete neurologic examination and, when appropriate, computed tomography and lumbar puncture. Specific CSF studies that may be of value include opening and closing pressures, cell count, glucose, protein, Gram stain, India ink stain, bacterial culture, viral culture, fungal culture, toxoplasmosis and cryptococcus antigen, and coccidioidomycosis titer. Even if the emergency department evaluation is unrevealing, all patients with new or changed neurologic signs or symptoms should be admitted to the hospital for further workup. The most common causes of neurologic symptoms include AIDS dementia, Toxoplasma gondii, and C. neoformans.

AIDS DEMENTIA AIDS dementia complex (also referred to as HIV encephalopathy or subacute encephalitis) is a progressive process commonly heralded by subtle impairment of recent memory and other cognitive deficits caused by direct HIV infection. In the early stages, diagnosis can be confused with depression, anxiety disorders, or substance abuse. Later phases of the illness are characterized by obvious changes in mental status and more severe disturbances, including aphasia and motor abnormalities. When a patient presents to the emergency department with an established diagnosis of AIDS dementia, with progressive signs or symptoms, it is important to rule out other CNS processes. A computed tomography (CT) scan in AIDS dementia typically shows cortical atrophy and ventricular enlargement.

TOXOPLASMOSIS Toxoplasmosis is the most common cause of focal encephalitis in patients with AIDS. Symptoms may include headache, fever, focal neurologic deficits, altered mental status, or seizures. Serologic tests are not useful in making or excluding the diagnosis because antibody to T. gondii is prevalent in the general population. The presence of antibody to T. gondii in the cerebrospinal fluid is helpful, although there is a high rate of false-negative results. On a noncontrast scan, toxoplasmosis typically appears as multiple subcortical lesions with a predilection for the basal ganglia.

Noncontrast CT scanning is often used as an initial imaging study in the emergency department in HIV-infected patients with neurologic deficits, since the addition of contrast has been shown to be of marginal value in patients with completely normal noncontrast CT scans. In cases in which clinical suspicion for CNS pathology is high but the CT scan is equivocal or negative, contrast enhanced CT scanning should be arranged in the emergency department. With contrast enhancement, toxoplasmosis lesions are ring-enhancing, with surrounding areas of edema. Magnetic resonance imaging is slightly more sensitive than contrast CT in detecting the extent and number of lesions with toxoplasmosis but is usually not indicated in the emergency department.

Other causes in the differential diagnosis of ring-enhancing lesions on contrast CT include lymphoma, fungal infection, and cerebral tuberculosis. In the emergency department, it is often not possible to differentiate these causes based on initial imaging studies, but general patterns in the appearance of lesions, based on underlying pathology, have been described. Toxoplasmosis tends to have a greater number of lesions with a predilection for the basal ganglia and corticomedullary regions, while lymphoma is more often characterized by singular lesions, typically in the periventricular white matter or corpus callosum. TB is distinguished by a characteristic inflammatory appearance on CT, with a thick, isodense exudate filling the basal cisterns.

Patients with suspected toxoplasmosis should be admitted and treated with pyrimethamine (100- to 200-mg load, then 50 to 100 mg/day) and sulfadiazine (4 to 8 g/day), with folinic acid added (10 mg/day) to reduce hematologic toxicity. Steroids are beneficial for significant edema or mass effect. Failure to improve suggests an alternative diagnosis, which may require biopsy. For patients responsive to toxoplamosis therapy, chronic suppressive therapy with pyrimethamine, sulfadiazine, and folinic acid is usually indicated after initial treatment. Oral TMP-SMX (1 DS qd) is recommended for prophylaxis in patients with positive toxoplasmosis serologic test results and CD4 cell counts less than 100 cells/pL.

CRYPTOCOCCOSIS Cryptococcal CNS infection may be seen in up to 10 percent of AIDS patients and may cause either focal cerebral lesions or diffuse meningoencephalitis. The most common presenting signs are fever and headache, followed by nausea, altered mentation, and focal neurologic deficits. Presentation may be subtle. Diagnosis relies on identifying organisms in cerebrospinal fluid by cryptococcal antigen (nearly 100 percent sensitive and specific), culture (95 to 100

percent sensitive), or staining with India ink (60 to 80 percent sensitive); serum cryptococcal antigen is also useful but has slightly lower sensitivity (approximately 95 percent). Patients with CNS cryptococcus shall be admitted for antibiotic therapy; preferred treatment is intravenous amphotericin B 0.7 mg/kg/day for 10 to 14 days. Oral flucytosine 100 mg/kg/day may be added to this therapy. Sixty percent of patients may be expected to respond to therapy, and side effects are frequent, most notably bone marrow suppression. Initial therapy should be followed by 8 to 10 weeks of oral fluconazole. Lifelong maintenance therapy with lower doses of fluconazole is indicated for all patients.

OTHER NEUROLOGIC DISORDERS Other, less common CNS infections that should be considered in the presence of neurologic symptoms include bacterial meningitis, histoplasmosis (usually disseminated), CMV, progressive multifocal leukoencephalopathy, herpes simplex virus, neurosyphilis, and TB. Noninfectious CNS processes include CNS lymphoma (occurring in 5 percent of AIDS patients and typically manifested as a subacute neurologic deterioration over several months), cerebrovascular accidents, and metabolic encephalopathies.

HIV infection is associated with a variety of disorders of the peripheral nervous system. The most common of these is HIV neuropathy characterized by painful sensory symptoms in the feet. Symptomatic relief with pain-modifying agents, such as amitriptyline or phenytoin, should be used judiciously because of their potential for causing delirium in patients with concurrent HIV dementia. Narcotic analgesia may be helpful in severe cases.

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