209 Neurological Manifestations of HIV 12 in two or more limbs or multiple cranial nerves as opposed to limited involvement in the early stage. The etiology of mononeuropathy multiplex in late HIV may be due to infec- tions such as herpes zoster, cryptococcus, toxoplasma and cytomegalovirus; and neoplastics such as lymphoma and cryoglobulinaemia. Treatment of mononeuropathy multiplex in late stage HIV includes antiretroviral therapy and treatment of under- lying infection. If no cause can be detected, empirical treatment with gancyclovir is recommended. Progressive polyradiculopathy occurs late in the course of HIV disease, and a large number of patients have coexisting cytomegalovirus (CMV) infection; how- ever, with effective antiretroviral therapy, the incidence of CMV-induced polyradiculopathy has declined. Patients present with radiating pain and paresthesias in cauda equina distribution resulting in cauda equina syndrome. Radiculopathy in upper limbs occurs in the late stage of disease. It has a poor prognosis with nearly 100% mortality within 30 days. Cerebrospinal fluid reveals raised protein and lym- phocytic pleocytosis. PCR may be positive for CMV DNA. Myelography and MRI demonstrate enhancement of lumbar thecal sac or leptomeninges in conus medullaris to cauda equina. Gancyclovir with other antiretroviral drugs is used for its treat- ment. Fig. 12.3a. Radiography of chest showing multiple lung abscesses in a 60 year old lady with AIDS (Courtesy Prof. U. K. Misra). 210 Tropical Neurology 12 Fig. 12.3b. Gadolinium enhanced spinal MRI, T 1 sequence in sagittal section of the same patient as in Figure 12.3a showing cervical vertebral involvement with prevertebral soft tissue shadow due to tuberculosis (Courtesy Prof. U. K. Misra). 211 Neurological Manifestations of HIV 12 Autonomic neuropathy seems to occur in late HIV disease, particularly when other neurologic deficits are present. Drugs such as tricyclic antidepressant, vincris- tine and pentamidine may contribute to autonomic dysfunction in HIV patients. On autopsy symptomatic and offending sympathetic ganglia have been found to be affected. Treatment is symptomatic and offending drugs should be withdrawn. Myopathy Progressive proximal muscle weakness is seen in late stage of HIV and is attrib- uted to wasting, cachexia, bacterial infections and antiretroviral drugs. Opportunistic infections in HIV Many opportunistic infections can affect the nervous system in AIDS patients which are mentioned in Table 12.3. Infection with HIV is associated with a broad spectrum of immune deficiency ranging from mild to severe. Susceptibility for op- portunistic infections and malignancies varies with degrees of immune suppression as indicated by peripheral blood CD4 lymphocyte counts; which are summarized in Table 12.4. To xoplasma Encephalitis To xoplasma is an intracellular parasite which exists in three forms: 1) Tachyzoites which causes active disease; 2) Bradyzoites responsible for latent disease; and 3) Oocyst- responsible for transmission of disease. Man acquires infection by ingesting oocyst shed in cat feces or ingesting bradyzoites in undercooked meat. In immunocompetent individuals, the primary infection remains asymptomatic in 90%. Toxoplasma encephalitis in HIV results due to reactivation of latent infection in 90% of patients and constitutes 60% of focal CNS mass lesions in HIV patients. Patients with toxoplasma encephalitis present with fever, headache and seizures. The patients may develop hemiparesis, ataxia and psychomotor retardation. HIV patients with toxoplasma encephalitis will have detectable serum antitoxoplasma IgG in 90-100% of patients. Antitoxoplasma IgM probably has little value in HIV patients. Cerebrospinal fluid PCR for toxoplasma is specific but not sensitive. CT scan reveals iso- or hyperdense lesions in the hemispheric gray-white junction, white matter or basal ganglia and 90% of lesions enhance as a ring or nodule (Fig. 12.4). If a single lesion is seen on MRI the likelihood of toxoplasma decreases to 34% and that of primary CNS lymphoma increases to 56%. On SPECT scan there is in- creased focal uptake in lymphoma and no uptake in toxoplasma and tuberculoma. Definite diagnosis of toxoplasma requires brain biopsy; however, a presumptive di- agnosis can be made on the basis of therapeutic improvement following py- rimethamine (100 mg po load, 75-100 mg four times daily and sulfadiazine 1.5-2 g qid) or pyramethamine and clindamycin (600-900 mg po qid). The clinical im- provement occurs in one to two weeks and radiological improvement occurs in two to three weeks. The primary treatment is continued for at least six weeks followed by chronic suppressive therapy for life. The suppressive therapy includes pyramethamine (20-50 mg po qid) and sulfadiazine (1 gm po tid) or clindamycin (300-400 mg po qid) and folinic acid (10-50 mg po qid). Clarithromycin and atovaquone have also been tried. In 50-70% of patients there are dose-limiting side effects. 212 Tropical Neurology 12 Cytomegalovirus (CMV) Encephalitis With the advent of highly effective antiretroviral therapy, the incidence of CMV infection has declined drastically in the developed countries but may be prevalent in developing countries. The CMV infection may be acquired through oral and respi- ratory secretion and contact with excreta, blood, semen and breast milk. About 80% of adults have antibodies against CMV, which is a member of the herpes virus group and may lie dormant in the CNS. The hallmark of CNS infection is a large cytomegalic (25-30 µm) cell containing a large central basophilic intranuclear in- clusion body looking like an owl’s eye as it is separated from the nuclear membrane by a halo. Autopsy studies reveal cytomegalic cells, discrete foci of parenchymal necrosis, microglial membranes and ventriculoencephalitis. CMV encephalitis presents with features of encephalopathy, confusion, disori- entation, apathy, psychomotor slowing and cranial nerve palsy. Ventriculoencephalitis begins with cognitive loss and apathy progressing within a few days or weeks to a state of withdrawn mutism and brainstem signs. Retinitis may also be present. MRI reveals enlarged ventricles, increased periventricular signal intensity on T 2 or both. CSF reveals mononuclear pleocytosis with elevated proteins. Culture of CSF for CMV is specific but insensitive. Detection of DNA by PCR in CSF is specific and sensitive. CMV infection may produce hyponatremia due to adrenalitis, which may be a clue to its diagnosis. Treatment of CMV encephalitis includes a combination of gancyclovir and foscarnet. Progressive Multifocal Leukoencephalopathy (PML) PML is caused by the JC virus infection. This virus is classified in the papova virus family. It is a ubiquitous virus that becomes reactivated from latency in the kidney. PML may be the first presentation of HIV. It is usually seen at CD4 counts less than 100/mm 3 . Symptoms can include limb weakness, cognitive dysfunction, visual loss, gait disturbance, lack of limb coordination, speech or language distur- bance and headache. CT scanning reveals hypodense white matter lesions without enhancement or edema. MRI lesions show increased signal attenuation on T 2 and decreased attenu- ation on T 1 . 13 CSF examination may yield a few WBCs and a normal opening pres- sure. JC virus PCR may be helpful in the diagnosis of PML since it has a sensitivity and specificity of 92%. 14-16 In situ hybridization may be useful for confirmation of PML. Autopsy reveals demyelination and giant astrocytes that are pleomorphic and have hyperchromatic nuclei. Oligodendrocytes appear altered with enlarged nuclei that stain abnormally dense with hematoxylin. These also may have ill-defined in- clusion bodies. 16 Table 12.3. Central nervous system infection associated with HIV Protozoa: Toxoplasma gondii , Trypanosoma cruzi , Acanthamoeba, Pneumocystis carinii Bacteria: Mycobacterium tuberculosis hominis , Trypanosoma pallidum , Mycobacterium avium complex, Listeria , Salmonella , pneumo- coccus, nocardia, mixed pyogenic bacteria Fungi: Cryptococcus neoformans , candida, aspergillus, coccidioides, histoplasma. Virus: Cytomegalo, herpes, varicella, J.C, Epstein-Barr, HSV8 213 Neurological Manifestations of HIV 12 Patients may have increased survival and improvement clinically with aggressive antiretroviral therapy. Ara-C or alpha interferon may be of some use, although its role is still controversial. Survival is poor with a mean of four months and maximum of 30 months. Primary CNS Lymphoma Lymphoma associated with HIV is largely B-cell lymphoma that may be related to the Epstein-Barr virus. Patients may present with symptoms of confusion, leth- argy, memory loss, hemiparesis and speech and language disorders. Seizures and cranial neuropathies are also seen. Lesions of primary CNS lymphoma commonly affect the deep white matter and are seen in the periventricular region, in the corpus callosum and the basal ganglia on CT scan and MRI. 9-10 Lymphoma can cross the corpus callosum. This propensity to cross may be helpful in differentiating lym- phoma from infectious etiologies that usually do not cross. Additionally, the CNS lymphoma seen in HIV has a higher rate of multicentricity and an increased rate of spontaneous central necrosis compared to lymphoma in non-HIV patients. PCR in the CSF may detect Epstein-Barr virus DNA. It may be difficult to distinguish the lesions of toxoplasma from those of lym- phoma on clinical grounds and neuro-imaging alone. 11 Hence, a therapeutic trial of toxoplasma may be undertaken as described above. The mainstay of the treatment of primary CNS lymphoma is whole brain radia- tion. Steroids can help to reduce the lesions. Survival is generally poor. Kaposi’s Sarcoma of the CNS Kaposi’s sarcoma, though rare, can cause lesions which present as cranial neuro- pathies, polyradiculopathy or myelopathy secondary to epidural metastasis with cord compression. Kaposi’s sarcoma is seen as a homogeneously enhancing mass lesion with mild edema. Stroke Hemorrhagic stroke may occur due to decreased platelets, ruptured mycotic an- eurysm and bleeding into an intracranial malignancy. Ischemic stroke may be seen in the setting of arteritis or endocarditis (bacterial or marantic). Patients with tuber- Table 12.4. Peripheral blood CD4 count and CNS infections Diseases CD4 cell count (cells/mm 3 ) >500 500-200 <200 <100 Syphilitic meningitis + + + + Tuberculous meningitis - + + + Cryptococcal meningitis - - + + Toxoplasma encephalitis - - + + Coccidioidal meningitis - - + + Progressive multifocal - - - + leukoencephalitis CMV encephalitis and - - - + radiculopathy Primary CNS lymphoma - - - + 214 Tropical Neurology 12 culosis can get a vasculitis that may cause basal ganglia infarcts. This is due to in- volvement of perforating arteries as these pass through infected basal cisterns. 12 Strokes are also seen with VZV (varicella zoster virus), fungal and bacterial infections (mu- cormycosis, aspergillosis, tubercular, syphilitic). Hypercoagulable states such as dis- seminated intravascular coagulopathy (DIC) and venous thrombosis due to dehydration can also cause stroke. It is unclear if there is an association between AIDS and stroke since intravenous drug addiction is a confounding variable in this population. Treatment of stroke and prevention of further events involves treatment of the underlying causes i.e., infectious versus hypercoaguable states. Rehabilitation therapy similar to regular stroke is advised. Fig. 12.4. Gadolinium enhanced cranial MRI on T 1 sequence in axial section showing ring ehancing lesions in basal ganglia and periventricular area in an AIDS patient with toxoplasma infection (courtesy of U. K. Misra). 215 Neurological Manifestations of HIV 12 HIV Infection in Children The prevalence of infection in children is highest in the tropics where the infec- tion is transmitted heterosexually. In 1994, 8% of AIDS patients in Uganda were below 12 years of age and 95% of them acquired infection from their mothers. The majority of these children became symptomatic before their first birthdays and more than 60% died before their second birthdays. Progressive encephalopathy is the most common manifestation of HIV infection in children manifesting with devel- opmental delay in motor and intellectual abilities, weakness and pyramidal signs. Children may have repeated bacterial infection, dementia, microcephaly and CNS opportunistic infection. CT and MRI reveal generalized brain atrophy and nonspe- cific T 2 hyperintensity. Antiretroviral therapy is the mainstay of the treatment along with treatment of coexisting infections. 17 Summary HIV infection is a rapidly spreading pandemic. Approximately 43 million people are infected with HIV worldwide and numbers are rapidly increasing. Neurological manifestations of HIV are well recognized. HIV affects all parts of the neuraxis including the central and peripheral nervous systems, meninges and the muscles. The central nervous system can be affected directly by HIV, i.e., ADC, PML and other opportunistic infections including bacterial, viral and fungal. In addition, pri- mary CNS lymphoma is also common in HIV. The pathogenesis of the many neu- rological syndromes associated with HIV is not well delineated. The diagnosis is dependent upon clinical presentation, blood tests, cerebrospinal fluid analysis, neuro-imaging studies and pathological studies of infected tissues. The treatment includes anti-retroviral agents as well as individual therapies customized to treat the individual opportunistic infections and antitumor treatment in appropriate neo- plastic conditions. Major emphasis must be on prevention of HIV particularly in underdeveloped countries. In spite of recent advances in the neurological manifesta- tion of HIV, there is a need for further basic, clinical, epidemiological and therapeu- tic research to eliminate this rapidly progressive pandemic. References 1. Snider W, Simpson D, and Nielson S et al. Neurological complications of acquired immune deficiency syndrome: Analysis of 50 patients. Ann Neurol 1983; 14:403-418. 2. Dal Pan GJ and McArthur JC. Neuroepidemiology of HIV infection. Neurologic Clinics 1996; 14:359-82. 3. Piot P, Tezzo R. The epidemiology of HIV and other sexually transmitted infec- tions in the developing world. Scand J Infect Dis (Suppl) 1990; 69:89-97. 4. Miller RF; Lucas SB; Hall-Craggs MA et al. Comparison of magnetic resonance imaging with neuropathological findings in the diagnosis of HIV and CMV asso- ciated CNS disease in AIDS. J Neurol Neurosurg Psych 1997; 62(4):346-51. 5. Price R, Brew B. The AIDS dementia complex. J Infect Disease 1988; 158:1079-1083. 6. Navia B, Jordan B, Price R. The AIDS dementia complex. I. Clinical Features. Ann Neurol 1986; 19:517-524. 7. Keating JM et al. Evidence of brain methyl transferase inhibition and early brain involvement in HIV positive patients. Lancet 1991; 337:935-939. 8. Brew BJ, Bhalla RB, Paul M et al. Cerebrospinal fluid β microglobulin in patients with AIDS dementia complex: An expanded series including response to Zidovudine treatment. AIDS 1992; 6:461-465. 216 Tropical Neurology 12 9. Santosh CG, Bell JE, Best JJ. Spinal tract pathology in AIDS: Postmortem MRI correlation with neuropathology. Neuroradiology 1995; 37(2):134-138. 10. Thurnher MM, Thurnher SA, Schindler E. CNS involvement in AIDS: Spectrum of CT and MR findings. European Radiology, 1997; 7(7):1091-1097. 11. Loberboym M, Estok L, Machac J et al. Rapid Differential Diagnosis of Cerebral To xoplasmosis and Primary CNS lymphoma by Thallium –201 SPECT. J Nucl Med 1996; 37:1150-1153. 12. Pinto A. AIDS and cerebrovascular disease. Stroke 1996; 27:538-543. 13. Provenzale, JM and Jinkins JR. Brain and spine imaging findings in AIDS pa- tients. Radiologic Clinics of North America 1997; 35:1127-65. 14. McGuire D, Barhite S, Hollander H et al. JC virus DNA in cerebrospinal fluid of HIV patients: Predictive value for PML. Ann Neurolog 1995; 37:395-399. 15. Price RW. Neurological complications of HIV infection. Lancet 1996; 348:445-52. 16. Stoner GL, Agostini HT, Ryschkewitsch CF et al. Detection of JC virus in two African cases of progressive multifocal leukoencephalopathy including identifica- tion of JCV type 3 in a Gambian IDS patient. J Med Microbiolog 1998; 47(8):733-742. 17. Katabira ET. HIV infection in the tropics. In: Chopra JS, Sawhaney IMS eds. Neurology in Tropics. New Delhi: Bichurchill Livingstone, 1999:127-139. CHAPTER 1 CHAPTER 13 Tropical Neurology, edited by U. K. Misra, J. Kalita and R. A. Shakir. ©2003 Landes Bioscience. Parainfectious Demyelinating Diseases of the Nervous System J. Kalita and U. K. Misra There is a wide spectrum of demyelinating diseases of the cerebral and periph- eral nervous systems which are temporally related to infection. These diseases are not due to direct injury by the organism as the neurological signs appear late in the course or weeks after recovery and the virus cannot be isolated from the neural tissues despite presence of inflammation and demyelination on histopathology. The post-infectious demyelinating syndromes are usually associated with virus-like ill- nesses but can also occur following immunization, bacterial infection, surgery and pyretotherapy. The spectrum of parainfectious demyelinating syndromes is wide and includes the following disorders: 1) acute disseminated encephalomyelitis; 2) acute hemorrhagic leukoencephalitis; 3) acute transverse myelitis; 4) optic neuritis; 5) cerebellitis; 6) Guillain Barre syndrome (GB Syndrome); and 7) brachial and lumbosacral plexopathy. Pathogenesis Parainfectious demyelinating disorders bear a striking resemblance to experi- mental autoimmune encephalomyelitis. The latter is an autoimmune response to the myelin basic protein and the proteolipid protein of the central nervous system (CNS). Cellular and humoral immune responses to myelin proteins occur, but the disease can be passively transferred only with sensitized lymphocytes in transgenic mice who are devoid of CD8 B cells and have only mature CD4 T cells. This experi- mental autoimmune encephalomyelitis suggests that antibodies are not critical for autoimmune encephalomyelitis. A number of mechanisms have been proposed to explain parainfectious demyelination: 1) direct viral effect; 2) virus induced im- mune mediated reaction; and 3) viral disruption of regulatory mechanisms of the immune system. Direct Viral Effect Demyelination due to direct viral effect may be attributed to virus infection of oligodendrocytes or Schwann cells. This results in demyelination through cell lysis or alteration in cell metabolism of the virus or viral product which may destroy the myelin membrane. Few viruses such as measles, mumps, influenza and varicella contain a fusion protein in their envelope. Fusion protein can dramatically alter the membranes, even of cells not susceptible to infection or after the virus has been inactivated by ultraviolet rays which may result in demyelinating changes. Myelin basic protein is an excellent substrate for protein kinase in the vaccine’s virus core. The release of this viral enzyme by a neighboring cell could have a profound effect on myelin structure and function. 218 Tropical Neurology 13 Virus-Induced Immune-Mediated Reaction In some viral infections, virus-specified polypeptides are introduced into the plasma membrane of the host cells. Antibodies or cell-mediated immune reactions against the viral antigen may destroy the host cell. If the host cell happens to be an oligodendrocyte or Schwann cell (myelin supporting cells), this may result in demy- elination. An alternative mechanism could be by exposing the sequestrated myelin antigen into the circulation following viral infection of myelin supporting cells. This results in an autoimmune response. Molecular mimicry has also been sug- gested to explain virus-induced immune-mediated demyelination. If virus polypep- tides share common antigenic determinants with central or peripheral nerve myelin, even a distant viral infection may trigger an autoimmune response against myelin. Molecular mimicry has been sought in the gene bank by looking for viral protein sequences resembling the encephalitogenic sequence in the myelin basic protein. Te r tiary structure and sequence alignment may lead to molecular mimicry such as a single T cell receptor can recognize distinct but structurally related peptides from different pathogens. Therefore, an encephalitogenic sequence of myelin protein might be mimicked by peptides of a variety of viruses, a phenomenon which can explain how diverse viral agents can induce demyelinating encephalomyelitis or polyneuri- tis. Parainfectious demyelination may also be due to an innocent bystander effect. During the inflammatory response evoked by a delayed hypersensitivity reaction, activated lymphocytes in macrophages release proteases or cytokines that can dis- rupt myelin, e.g., intracerebral inoculation of tuberculin-purified protein to a tu- berculin-sensitized guinea pig results in demyelination accompanied by inflammatory response at the site of inoculation. Similarly an immune reaction against a viral antigen in the vicinity of central or peripheral myelin can result in demyelination without concomitant infection of myelin-supporting cells. Viral Disruption of Regulatory Mechanism of the Immune System The phenomenon of self-tolerance was thought to result from deletion of the potential “self” reactive clones of lymphocytes at an early age. Tolerance, however, is an active process in which autoimmune reactions are suppressed by regulatory mecha- nisms of the immune system. Infections may precipitate autoimmune disease by perturbating immunoregulatory mechanisms resulting in immune-mediated parainfectious demyelination. Several mechanisms have been postulated for parainfectious demyelination. An antecedent viral infection could increase the vulnerability of nervous tissue to attack from a previously persistent subclinical autoimmune process. Alternatively, viral in- fection of the myelin sheath or the myelin supporting cell could alter the pattern of myelin breakdown. This can result in a disturbance of balance to trigger the autoim- mune process. The most attractive hypothesis of parainfectious demyelination is that the virus directly acts on T cell subsets, receptors disturbing the balance that normally prevents a symptomatic autoimmune reaction. Measles and the Epstein- Barr virus, which are the commonest viruses related to acute disseminated encepha- lomyelitis and Guillain-Barre syndrome, respectively, alter T cell activity during primary infection. [...]... sclerosis and paranfectious events Arch Neurol 1993; 50 :53 2 -5 35 Hoffman HL Acute necrotic myelopathy Brain 1 955 ; 78:37 7-3 99 Kalita J, Misra UK, Mandal SK Prognostic predictors of acute transverse myelitis Acta Neurol Scand 1998; 98:6 0-6 2 Kalita J, Misra UK Postural hypotension in a patient with acute transverse myelitis Post Graduate Med J 1996; 72:18 0-1 82 Choi KH, Lee KS, Chung SO et al Idiopathic transverse... no specific treatment for idiopathic ATM Prednisolone ( 1-1 .5 mg/kg/ day for 7-1 4 days), adrenocorticotrophic hormone (4 0 -5 0 units daily for 7-1 0 days) or a high dose of intravenous methyl prednisolone (50 0 mg I/V for 5 days) have been used without consistent benefits Supportive care of ATM includes prevention of deep venous thrombosis by heparin 50 00 units subcutaneously twice daily; prevention of bed... Epidemiol 19 85; 4:13 8-1 45 Bortone E, Be Honi L, Buzio S, Disoldato S et al Spindle coma and alternating pattern in the course of measles encephalitis Clin Electroencephalogra 1996; 27:21 0-2 14 Ipsen P CT variefied intracranial calcifications and contrast enhancement in acute disseminated encephalomyelitis A case report Pediatr Radiol 1998; 28 :59 1 -5 93 Jaffery DR, Mandler RN, Davis L Transverse myelitis-retrospective... myelitis: MR characteristics Am J Neuroradiol 1996; 17:1 15 1-1 160 Hafer-Macko CE, Seikh KA, Li CY et al Immune attack in the Schwann cell surface in acute inflammatory demyelinating polyneuropathy Ann Neurol 1996; 39:62 5- 6 35 Asbury AK, Arnason BGW, Adams RD The inflammatory lesion in idiopathic polyneuritis Medicine (Baltimore) 1969; 48:17 3-2 50 French Cooperative group on plasma exchange in Guillain... Diaphragmatic palsy may accompany in 6% of patients Bilateral signs and symptoms may be present in 2 5- 3 0% of patients Recurrence of symptoms may be present in 1 -5 % 13 236 Tropical Neurology Pathophysiology The pathophysiology and pathogenesis of this disorder is not clear, but abruptness of onset is consistent with immune-mediated disease Rapid recovery in some patients may suggest a demyelinating etiology The... China The spectrum of neuropathological changes Brain 19 95; 118 :57 7 -5 95 Subramony SH AAEM case report #14 neurologic Amyotrophy (Acute brachial neuropathy) Muscle Nerve 1988; 11:3 9-4 4 13 CHAPTER 14 Fungal Infections of the Central Nervous System David Saffer and Raymond A Smego, Jr Fungal infections of the central nervous system (CNS) occur in both tropical and temperate regions of the world, although... serum protein electrophoresis, HIV, HTLV-1, test for tuberculosis and serum B12 levels Peripheral leukocytosis is present in one-third of patients at the onset of ATM Cerebrospinal fluid analysis reveals mild to moderate protein rise (10 0 -5 00 mg/dl) and mononuclear pleocytosis (below 100/mm3) Occasionally CSF may be normal Partial myelographic block may be present in 5% of patients due to cord swelling... syndrome plasmapheresis and IV Ig are useful References 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Stuve O, Zamvir SS Pathogenesis, diagnosis and treatment of acute disseminated encephalomyelitis Curr Opin Neurolog 1999; 12:39 5- 4 01 de Quadros CA, Hersh BS, Nogrreira AC et al Measles eradication: Experiences in the Americas Bull WHO 1998; 76:4 7 -5 2 Murphy J, Austin J Spontaneous infection or vaccination as... plasma exchanges in the Guillain Barre syndrome Ann Neurol 1997; 41:29 8-3 06 Asbury AK, McKhann GM Changing views of Guillain Barre syndrome Ann Neurol 1997; 41:28 7-2 88 Ho TW, Li CY, Gao CY et al Guillain Barre syndrome in northern China The relationship to campylobacter Jenuni infection and antiglycolipid antibodies Brain 19 95; 118 :59 7-6 05 Griffin JW, Licy HTW, Macko XC et al Guillain Barre syndrome in... six months one patient died, 15 had a poor outcome and 15 had a good outcome.8 Guillain-Barre Syndrome Guillain-Barre (GB) syndrome is an acute inflammatory demyelinating polyradiculoneuropathy The majority of these cases follow a virus-like illness The annual incidence is one to two cases/100,000 population The latent period between prodromal symptoms related to virus-like illnesses in the respiratory . meningitis - - + + Progressive multifocal - - - + leukoencephalitis CMV encephalitis and - - - + radiculopathy Primary CNS lymphoma - - - + 214 Tropical Neurology 12 culosis can get a vasculitis. (cells/mm 3 ) > ;50 0 50 0-2 00 <200 <100 Syphilitic meningitis + + + + Tuberculous meningitis - + + + Cryptococcal meningitis - - + + Toxoplasma encephalitis - - + + Coccidioidal meningitis - - + + Progressive. pyramethamine (2 0 -5 0 mg po qid) and sulfadiazine (1 gm po tid) or clindamycin (30 0-4 00 mg po qid) and folinic acid (1 0 -5 0 mg po qid). Clarithromycin and atovaquone have also been tried. In 5 0-7 0% of patients