Neurological Manifestations             of Human Immunodeficiency           VirusPresenter - Dr.Garima AggarwalModerator -...
 HIV is the most common viral infection of the nervous  system, affecting both the CNS and PNS. Upto 50% of HIV patients...
NEUROPATHOGENESIS          Nervous System effects of HIV infection     DIRECT                          INDIRECTHIV virus a...
NEUROPATHOGENESIS
CLASSIFICATION OF NEUROLOGICAL MANIFESTATIONS                               OF HIVHIV can involve disorders of both the CN...
Neurological Manifestations of HIV           involving the               BRAIN         *AIDS defining illnesses are marked...
• HIV Encephalopathy/ ADC                • Progressive Multifocal Leuco-    DEMENTIA      Encephalopathy                • ...
•   CMV Encephalitis                   •   PMLE                   •   HSV , VZV    ENCEPHALITIS   •   Toxoplasma Encephali...
Neurological Manifestations of HIV           involving the          MENINGES
M             • HIV Seroconversion Illness-                Aseptic meningitisE   ACUTE     • Pneumococcal, MeningococcalN ...
Neurological Manifestations of HIV           involving the         SPINAL CORD
M   HIV associated   • Vacoular MyelopathyYE                    •   CMV Myelopathy                     •   Varicella Zoste...
Neurological Manifestations of HIV           involving the     PERIPHERAL NERVES
•   AIDP                         •   CIDPN    EARLY STAGES-       Immune                         •   Vasculitic Neuropathy...
Neurological Manifestations of HIV           involving the           MUSCLES
•   HIV PolymyositisM                  •   CMV PolymyositisY    INFECTION     •   Pyomyositis                   •   AIDS c...
Some commonly encountered Neurological Manifestations          Of HIV    In Clinical Practice
ASEPTIC HIV MENINGITIS 10-15% of patients with Acute HIV Seroconversion illness present  with meningtisPATHPHYSIOLOGY – ...
ASEPTIC MENINGITIS continued INVESTIGATIONS1. LP – CSF sugar - Normal                           (40-70mg/dl)             ...
HIV ENCEPHALOPATHY/                AIDS DEMENTIA COMPLEX     In the era of HAART, 10-20% of HIV patients are affected by ...
HIV ENCEPHALOPATHY continuedCLINICAL FEATURESCognitive impairment – Forgetfulness                       Decreased Attenti...
 There are no specific diagnostic criteria for HIV Encephalopathy. Diagnosis of dementia – demonstrating a decline in co...
INVESTIGATIONS – testing done only to exclude other diagnosis1. Neuropsychological testing – MMSEIt is advisabele in all ...
TREATMENT HAART – HAART improves neuropsychological performance  (Larussa etal 2006)         - upto 50% reduction in HIV...
CRYPTOCOCCAL MENINGITIS Initial AIDS defining illness in 2% of patients More common with CD4+ T cell count of <100/mic.l...
INVESTIGATIONS1. CT/MRI – Hydrocephalus                                               Complications of              Gelat...
CT brain showing -1.GelatinousPseudocyst( formed byconfluence of dilatedperivascular spaces).2.Sites: Basalganglia, cerebr...
TREATMENT                  Amphotericin B   +/- Flucytosine          (0.5 to 0.7 mg/kg/day)    ( 75 to 150 mg/kg/day) Re...
TOXOPLASMOSIS of the BRAIN Associaterd with CD4+T cell count < 100cells/micr.l Most commmon cause of focal intracranial ...
INVESTIGATIONS1. CT / MRI – ‘Multiple lesions in Multiple Locations’             Ring Encancing Lesions – inflammation an...
D/D of Ring Enhancing Lesions
e   d
TREATMENT                 Sulfadiazine + Pyrimethamine     (05 to 1.5g P/O q 6th hrly) (200mg loading dose Day 1)        ...
PROGRESSIVE MULTIFOCAL LEUCOENCEPHALOPATHY It is a late manifestation, seen in 4% of patients with AIDSPATHOGENESISCause...
INVESTIGATIONS1. CT / MRI – Multiple nonenhancing white matter lesions,              may coalesce, predilection for occip...
FLAIR Images ShowingProgression of ProgressiveMultifocal Leukoencephalopathy a) Multifocal, high-signal-intensity lesions ...
T2 flair MRI brain shows White matter hyperintensity of subcortical U fibers, splenium ofcorpus callosum in posterior cer...
TREATMENT No specific therapy available for PMLE Improved survival has been seen with HAART                           H...
PRIMARY CNS LYMPHOMA Complicate the course of AIDS in upto 5% of patients.PATHOGENESISPCNSL of B cell origin are conside...
INVESTIGATIONS1. MRI > CT – one or more deep lesions              - location – deep, adjacent to lateral ventricle       ...
A)POST CONTRAST T1WI    B) FLAIR T2WI    A-B. 24 year-old man with AIDS                                        Show a soli...
TREATMENT HAART – vigorous attempts to suppress HIV replication are  recommended in all patients with PCNSL Mass effect...
VACUOLAR MYELOPATHY VM is the most common cause of spinal cord dysfunction in  untreated patients with AIDS. It is appar...
VACUOLAR MYELOPATHY                             VITAMIN B12- sacd  S. Vitamin B12 levels are Normal                       ...
INVESTIGATION nonspecific , to exclude other etiologies1. MRI SPINE – Cord swelling wtith intramedullary enhancement     ...
Sagittal T2-weighted                       images of the cervicalC2                     spine-     Iintramedullary     sig...
HIV associated NEUROPATHY    Peripheral neuropathies complicate all stages of HIV.    Symptomatic neuropathy is seen in ...
DISTAL SENSORY POLYNEUROPATHYCLINICAL FEATURES Painful burning sensation, with numbness in both feet.Hands spared Depre...
Thank you
References1. Neurology in Clinical Practice – 3rd edition(Bradley, Daroff, Fenchal)2. Adams and Victor’s Principles of Neu...
Neurological manifestations of HIV
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Neurological manifestations of HIV

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A brief description of the many neurological manifestations of HIV infection.

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Neurological manifestations of HIV

  1. 1. Neurological Manifestations of Human Immunodeficiency VirusPresenter - Dr.Garima AggarwalModerator - Dr (Brig) Rajesh Kakkar Dr.Manish Mittal
  2. 2.  HIV is the most common viral infection of the nervous system, affecting both the CNS and PNS. Upto 50% of HIV patients have clinically apparent neurological disease. Upto 20% of HIV patients present for the first time with neurological manifestations. Upto 90% of HIV patients have neuropathological changes on autopsy. India has the second largest burden of HIV related pathology next to sub-Saharan Africa. Neurological complications associated to HIV-1 infections, are very common in our clinical setting.
  3. 3. NEUROPATHOGENESIS Nervous System effects of HIV infection DIRECT INDIRECTHIV virus and its products Oppurtunistic infections HIV associated NeoplasmsCells affected by HIV - Perivascular Macrophages Monocytes from blood Microglial cells ?Astrocytes
  4. 4. NEUROPATHOGENESIS
  5. 5. CLASSIFICATION OF NEUROLOGICAL MANIFESTATIONS OF HIVHIV can involve disorders of both the CNS and PNS.Classification based on the neuroanatomical localization and clinical syndromes associated - BRAIN Dementia Space occupying lesions Encephalitis Stroke like syndromes MENINGES Meningitis SPINAL CORD Myelopathy Radiculopathy PERIPHERAL NERVES Peripheral Neuropathy Inflammatory Demyelinating Polyneuropathies Toxic Neuropathy MUSCLE Polymyosistis , Pyomyositis HIV associated Wasting Syndrome
  6. 6. Neurological Manifestations of HIV involving the BRAIN *AIDS defining illnesses are marked in RED
  7. 7. • HIV Encephalopathy/ ADC • Progressive Multifocal Leuco- DEMENTIA Encephalopathy • Tuberculosis • NeurosyphilisB • LymphomaR • Abscesses Tuberculosis ListeriaA Nocardia E.ColiI • Infective Granulomas ToxoplasmaN SPACE Aspergillus OCCUPYING Candida Cryptococcus LESIONS • Neoplastic Primary CNS Lymphoma Secondary Metastasis Metastatic Kaposi’s Sarcoma Glioma • Others PMLE, Varicella Zoster, CMV
  8. 8. • CMV Encephalitis • PMLE • HSV , VZV ENCEPHALITIS • Toxoplasma Encephalitis • Aspergillus encephalitisB • • Metabolic Encephalitis IRISR IA • Granulomatous Angitis – AIDS associated • Infectious Vasculitis – Tb, Neurosyphilis, S CI Aspergillus, Mucor • Varicella Zoster Virus Vasculitis H E • Bacterial Endocarditis, non bacterial thromboticN STROKE Like endocarditis M I Syndromes • Venous thrombosis – Hypercoagulable states C • HIV asso. Thrombocytopenia • DIC H • METASTATIC- Kaposi’s Sarcoma, PCNSL E • Coagulopathy M O.
  9. 9. Neurological Manifestations of HIV involving the MENINGES
  10. 10. M • HIV Seroconversion Illness- Aseptic meningitisE ACUTE • Pneumococcal, MeningococcalN • E.Coli • KlebsiellaI • ListeriaNG • Mycobacterium tuberculosis • Mycobacterium Avium complexI • Cryptococcus • CandidaT CHRONIC • SyphilisI • Nocardia • Metastatic Meningitis -S Lymphoma
  11. 11. Neurological Manifestations of HIV involving the SPINAL CORD
  12. 12. M HIV associated • Vacoular MyelopathyYE • CMV Myelopathy • Varicella Zoster VirusL INFECTIONS • Herpes Simplex Virus • HTLV 1 and 2O • NeurosyphilisP NEOPLASTIC • Lymphoma/metastasis associatedA MyelopathyTH METABOLIC • Vitamin B 12 DeficiencyY
  13. 13. Neurological Manifestations of HIV involving the PERIPHERAL NERVES
  14. 14. • AIDP • CIDPN EARLY STAGES- Immune • Vasculitic Neuropathy • Cranial MononeuropathyE Dysregulation • Multiple mononeuropathies • Plexopathy – Brachial, LumbosacralU MID STAGE – HIV • Distal Sensory PolyneuropathyR Replication driven • Autonomic NeuropathyO • CMV polyradiculopathy, Mononeuritis MultiplexP LATE STAGES – • Syphilitic Polyradiculomyelitis Oppurtunistic • Tuberculous PolyradiculomyelitisA Infections, Neopla • Zoster ganglionitis • Lymphomatous Polyradiculopathy smsT • AIDS Cachexic neuropathy • ALS like motor neuropathyH • Nucleoside Reverse Transcriptase Inhibitors – ALL STAGES (TOXIC Didanosine, Zalcitabine, StavudineY NEUROPATHY) • Other Concomittantly used drugs – Vincristine, Isoniazid, Ethambutol, Thalidomide
  15. 15. Neurological Manifestations of HIV involving the MUSCLES
  16. 16. • HIV PolymyositisM • CMV PolymyositisY INFECTION • Pyomyositis • AIDS cachexia- HIV associatedO Wasting SyndromePAT • ZIDOVUDINEH DRUG INDUCED • Others especially NRTISY
  17. 17. Some commonly encountered Neurological Manifestations Of HIV In Clinical Practice
  18. 18. ASEPTIC HIV MENINGITIS 10-15% of patients with Acute HIV Seroconversion illness present with meningtisPATHPHYSIOLOGY – Immune mediated illnessCLINICAL FEATURESHeadache – severe and protracted, isolated persistant headacheSigns of meningeal irritation – nausea, vomiting, photophobiaAcute Seroconversion illness – Flu like febrile illnessPreserved alertness and cognitionMay be associated with features of EncephalitisCranial nerve Involvement may be seen – CN VII, rarely V and/or VIIIIt is a diagnosis of exclusion.
  19. 19. ASEPTIC MENINGITIS continued INVESTIGATIONS1. LP – CSF sugar - Normal (40-70mg/dl) protein - Elevated but <100mg/dl (15-50mg/dl) cells - lymphocytic pleocytosis (0-5 Mono/mm3)2. Intrathecal anti HIV IgG3. Serum P 24 capture assay, HIV RNA level TREATMENTNo specific therapy is needed.Resolves in 2-4 months without treatment.
  20. 20. HIV ENCEPHALOPATHY/ AIDS DEMENTIA COMPLEX  In the era of HAART, 10-20% of HIV patients are affected by it.  It is the first manifestation of AIDS in upto 3 % of HIV patients  Associated wth CD4+ T cell count of < 200/mm3  It s considered part of the HIV associated Neurocognitive Impairment spectrum Minor Cognitive Motor Assymptomatic AIDS Dementia Complex DysfunctionHIV associated NCI, progresses with increased viral load and immunosuppression PATHOGENESIS – neuropathogenesis as described above. White matter – pallor, multinucleated cell encephaltis, vacoular changes, focal necrosis and neuronal loss. The cerebral cortex is relatively spared. Areas affected- subcortical structures of brain and spinal cord.
  21. 21. HIV ENCEPHALOPATHY continuedCLINICAL FEATURESCognitive impairment – Forgetfulness Decreased Attention and Concentration Inability to perform complex task Decreased Sexual drive and disrupted Sleep Mild mania and AgitationMotor Dysfunction- Poor balance Gait incoordination- slow and rigid gait Slowness of movements Postural tremors Choreoform movements, myoclonic jerksVegetative state- Bowel and Bladder incontinence Unable to Ambulate lying in bed mute with vacant stare
  22. 22.  There are no specific diagnostic criteria for HIV Encephalopathy. Diagnosis of dementia – demonstrating a decline in cognition CLINICAL STAGING OF HIV ENCEPHALOPATHY STAGE Mental Function Motor Function STAGE 0 Normal NormalSTAGE 0.5 Absent, Minimal or Equivocal Slowed ocular and extremity symtoms movements STAGE 1 Able to perform all but the Unequivocal motor demanding aspects.Unequivocal impairment func. and intellectual impairment Can walk without assistance STAGE 2 Performs basic self care Ambulatory Cannot work or maintain May require a single prop demanding aspects of daily life STAGE 3 Major Intellectual incapacity Major motor disability Cannot walk unassisted STAGE 4 Intellect, social comprehension and Paraparetic or paraplegic with output at rudimentray level bowel, bladder incontinence
  23. 23. INVESTIGATIONS – testing done only to exclude other diagnosis1. Neuropsychological testing – MMSEIt is advisabele in all patients with HIV to have a baseline MMSE.2. CT / MRI - Diffuse cerebral atrophy Patchy or diffusely abnormal signals esp on FLAIR – (Hemispheric white matter +/- basal ganglia and thalamus) Basal Ganglia calcification – in children Non specific 3.CSF findings – sugar - normal CSF changes protein - mildly elevated cells - lymphocytic pleocytosis special tests – HIV IgG synthesis Oligoclonal bands HIV DNA amplification Quantitative CSF-HIV Burden others MCP1, neopterin, Quin. Acid, Beta2MGThe practical utility of special CSF testing is uncertainNo absolute correlation exists between CSF HIV burden and disease severity
  24. 24. TREATMENT HAART – HAART improves neuropsychological performance (Larussa etal 2006) - upto 50% reduction in HIV enceph. since HAART - simpler regimens with least number of drug side effects - Drugs with high CSF penetration should be used (Zidovudine, Stavudine, Lamivudine, efavirenz, nevirapine) Neuroleptic medication- for patients with psychobehavorial dys. - they have increased sensitivity to EPS side effects of neurleptic drugs - TCAs and SSRIs - Clozapine and Haloperidol Anticonvulsant – Gabapentin and topiramate are preferred Psychological support, assisted living.
  25. 25. CRYPTOCOCCAL MENINGITIS Initial AIDS defining illness in 2% of patients More common with CD4+ T cell count of <100/mic.l CLINICAL FEATURES Subacute onset Signs of meningeal irritation – fever, stiff neck,vomiting, photophobia Cryptococcomas and Cranial nerve involement rarely Head to Toe examination for associated infection Skin lesions, like Molluscum contagiosum Palatal and oral ulcers Myocarditis Pulmonary involvement – in 1/3rd of case Gastroenteritis Prostatitis – prostate may serve as reservoir for smoldering infection
  26. 26. INVESTIGATIONS1. CT/MRI – Hydrocephalus Complications of Gelatinous pseudocysts Cryptoccal Cryptococcomas meningitis only nonspecific Cerebral Atrophy2. CSF - sugar - decreased D/D TbM protein - elevated protein cells - monomuclear pleocytosis India ink smear – nonspecific D/D Aspergillus, C.immitus, Candida, H.Capsulatum, Naeglaeria CSF cryptococcal antigen (CrAg) – sensitivity 95% Fungal CSF culture for Cryptococcus – gold standard
  27. 27. CT brain showing -1.GelatinousPseudocyst( formed byconfluence of dilatedperivascular spaces).2.Sites: Basalganglia, cerebralcortex, cerebellumand midbrain. No contrastenhancementMRI: Cyst are of CSFintensity
  28. 28. TREATMENT Amphotericin B +/- Flucytosine (0.5 to 0.7 mg/kg/day) ( 75 to 150 mg/kg/day) Renal insufficiency Hematological Hypokalemia x 2 to 3 weeks Toxicity Hypomagnesemia Fluconazole 200mg P/O BD x upto 3 monthsMaintainence therapy -Fluconazole 200mg P/D OD (1st line) Amphotericin/Itraconazole weekly (2nd line) Continue till the CD4+T cell count >200cells/micr.l Increased ICP – Medical- corticosteroids and Acetazolamide Repeated Lumbar punctures, VentriculostomyAcute mortality approaches 30% and is related to inceased ICP
  29. 29. TOXOPLASMOSIS of the BRAIN Associaterd with CD4+T cell count < 100cells/micr.l Most commmon cause of focal intracranial masses in patients with AIDSPATHOGENESISIt almost always occurs as a Recrudescence of previously acquired infection.It is 10 times times more commmon in patients with Ab to Toxoplas.CLINICAL FEATURES FEVER HEADACHE FOCAL NEUROLOGICAL DEFICITS (Seizures/Hemiparesis/Aphasia)Rarely patient may have Confusion, Dementia, Lethargy or Coma
  30. 30. INVESTIGATIONS1. CT / MRI – ‘Multiple lesions in Multiple Locations’ Ring Encancing Lesions – inflammation and central necrosis2. IgG Ab to Toxoplasma – This should be done for all HIV patients at the time of initial workup.3. Brain Biopsy – only confirmatory test - patients with failed 2-4 weeks of antitoxoplasma therapy
  31. 31. D/D of Ring Enhancing Lesions
  32. 32. e d
  33. 33. TREATMENT Sulfadiazine + Pyrimethamine (05 to 1.5g P/O q 6th hrly) (200mg loading dose Day 1) ( 75mg P/O OD maintainence) With Folinic Acid (10mg/day)Long term Suppressive therapy – Sulfadiazine + Pyrimethamine (2g/day) (25mg/day) May need to continue maintainence therapy life long in some Or until CD4+T cell count > 200cells/micr.lProphylaxis – HIV ,CD4+Tcell count <100c/mi.l, IgG toxoplasma +vePrimary Prevention – HIV , but seronegative for toxoplasma
  34. 34. PROGRESSIVE MULTIFOCAL LEUCOENCEPHALOPATHY It is a late manifestation, seen in 4% of patients with AIDSPATHOGENESISCaused by the JC virus, DNA containing HPV. Only known complicationApprox 90% of general adult population is already exposed to this virus in early childhood, and contains antibodies against it.Lesions – small foci of demyelination in subortical white matter, which coalesce. Areas – Occipital and parietal lobes, cerebellum, brainstem and rarely Spinal Cord.CLINICAL FEATURES Protracted course Multifocal Neurological deficits - Seizures Visual Field defects Aphasia Ataxia, and occ. Sensory deficits With or without mental status changes
  35. 35. INVESTIGATIONS1. CT / MRI – Multiple nonenhancing white matter lesions, may coalesce, predilection for occipital and parietal. MRI – decreased signal intensity on T1 - Hyperintensity on T22. CSF – non specific changes - CSF PCR for JC virus DNA (sensitivity 76%, specificity 100%)3. Brain Biopsy – if clinical diagnosis likely, but no viral DNA detected on CSF Bizarre giant astrocytes with pleomorphic hyperchromic nuclei Altered oligodendrocytes with enlarged nuclei Cells with viral inclusions and myelin loss
  36. 36. FLAIR Images ShowingProgression of ProgressiveMultifocal Leukoencephalopathy a) Multifocal, high-signal-intensity lesions (arrow) in theright hemisphere of a patient TheCSF was positive for JC virus. b) Contrastenhancement is not evident(arrow). c ) 6 weeks later, progressionof the white matter lesions(arrow) shows involvement of theuncinate fibers. d )Patchy enhancement withgadolinium (arrow) is noted (predominantlyin the right hemisphere
  37. 37. T2 flair MRI brain shows White matter hyperintensity of subcortical U fibers, splenium ofcorpus callosum in posterior cerebral hemisphereNo contrast enhancementNo mass effectCommon sites: temporal and occipital white matter, Subinsular region, corpus callosumand subcortical U fibers
  38. 38. TREATMENT No specific therapy available for PMLE Improved survival has been seen with HAART HIV with PMLE without HAART with HAARTMean Survival- 3 – 6 months around 2.5 years (>7years*) Patients on HAART may show paradoxical worsening due to IRISOnly 50% of patients on HAART show any neurological improvement Other therapies tried – Cytosine, acyclovir, Vidrabine, IFN alpha All these therapies have shown generally unsatisfactory results
  39. 39. PRIMARY CNS LYMPHOMA Complicate the course of AIDS in upto 5% of patients.PATHOGENESISPCNSL of B cell origin are considered oppurtunistic neoplasms.CLINICAL FEATURESSimilar to Toxoplasmosis – fever, headache , FNDs PCNSL TOXOPLASMA Tempo of evolution slower presents as acute/subacute several days to few weeks Fever usually absent may or maynot be present No response to antitox therapy Show clinical and neuroimaging imrovement in response to Antitox therapy
  40. 40. INVESTIGATIONS1. MRI > CT – one or more deep lesions - location – deep, adjacent to lateral ventricle - White matter rather than gray matter - subependymal extension - predilection for Posterior fossa - Mass effect may be present, surrounding edema rare2. CSF – unhelpful - Monoclonal B lymphocytes by flowcytometry Corroborative evidence on - CSF – EBV virus DNA amplification PCNSL3. BRAIN BIOPSY – definitve diagnosis - After a failed therapeutic trial for Toxoplasmosis4. SPECT SCAN – may be useful.
  41. 41. A)POST CONTRAST T1WI B) FLAIR T2WI A-B. 24 year-old man with AIDS Show a solitary large ring-enhancing lesion with mild mass effect and moderate vasogenic edema. The hypointensity of the lesion on T2WI is characteristic of lymphoma. Note that the mass effect and edema is less than expected given the size of the lesion, as is typical for primary brain lymphoma while much more edema and mass effect vs. lesion size is expected in toxoplasmosis.C) POSTCONTRAST T1WI D) T2WI C-D. 30 year-old man with AIDS show left temporal lobe vasogenic edema, related to a temporal lobe mass lesion (not shown). There are also bilateral lesions in the caudate nuclei on T2WI (D)(red), with periventricular and ependymal extension of enhancement on the right (C).(green) The ependymal spread is characteristic of PCNSL
  42. 42. TREATMENT HAART – vigorous attempts to suppress HIV replication are recommended in all patients with PCNSL Mass effect – High dose corticosteroid therapy Radiotherapy – Palliative whole brain radiotherapy Chemotherapy – Its use remains controversial, trial stages.
  43. 43. VACUOLAR MYELOPATHY VM is the most common cause of spinal cord dysfunction in untreated patients with AIDS. It is apparent in 25% to 55% of AIDS autopsy series It frequently coexists with HIV Encephalopathy and Distal Sensory polyneuropathyCLINICAL FEATURES Subacute onset – over weeks or months Gait disturbances, imbalance Ataxia Spasticicity Sphincter dysfunction Examination –Spastic parapareis, Hyperreflexia, Babinski +ve, Loss of proprioception and vibration sense . No sensory level. Arms are typically spared
  44. 44. VACUOLAR MYELOPATHY VITAMIN B12- sacd S. Vitamin B12 levels are Normal DecreasedUsually associated with Distal Sensory Not seen neuropathy Vacoular changes in myelin sheaths Decreased methylation of histidine and phasphatidylcholine prod. HIV infected patients may also present with Vitamin B 12 deficiency.
  45. 45. INVESTIGATION nonspecific , to exclude other etiologies1. MRI SPINE – Cord swelling wtith intramedullary enhancement - T2 signal changes2. CSF – testing for Viral DNA – CMV, VZV, HSV, HTLV 1 & 2TREATMENT HAART – Viral control can result in improved neurological function is not well documented in VM. Assistance – Personal Care of neurogenic bladder, bladder infection Prevention of skin breakdown Management of limb spasticity, etc.
  46. 46. Sagittal T2-weighted images of the cervicalC2 spine- Iintramedullary signal  increased signal on T2C5 enhancement extending from C2 though approximately C5. The axial T2 image-  Abnormal signal to be symmetric within the posterior columns of the cord.
  47. 47. HIV associated NEUROPATHY  Peripheral neuropathies complicate all stages of HIV.  Symptomatic neuropathy is seen in 10-15% of patients but pathological changes of peripheral nerve involvement - almost all AIDS patients HIV ass. NEUROPATHYDistal Sensory CMV assoc. NRTI assoc. TOXIC AIDP and CIDP PN POLYRADICULOPATHY NEUROPATHY
  48. 48. DISTAL SENSORY POLYNEUROPATHYCLINICAL FEATURES Painful burning sensation, with numbness in both feet.Hands spared Depressed or absent ankle jerks, mild pain, temp., vibratory sense loss in the feet. Symmetrical involvement is a characteristic clinica feature and hands are usually spared.INVESTIGATIONS – typical clinical features are diagnosticTREATMENT Reduce exposure to NEUROTOXINS – Ethanol, NRTIs, INH, Metronidazole, Dapsone, Vincristine Screen for Vitamin B 12 Deficiency, Diabetes Mellitus HAART Pain control – TCAs – Nortiptyline > Amitriptyline Help relieve - Anticonvulsants – Gabapentin neuropathic pain
  49. 49. Thank you
  50. 50. References1. Neurology in Clinical Practice – 3rd edition(Bradley, Daroff, Fenchal)2. Adams and Victor’s Principles of Neurology- 9th edition3. Harrison’s principles of Internal Medicine – 17th edition4. Textbook of neurology- Dounghey5. NACO guidelines for management of AIDS- 20106.WHO guidelines for HIV/AIDS7. World Wide Web
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