This document summarizes neurological manifestations of human immunodeficiency virus (HIV). It discusses how HIV can affect both the central nervous system and peripheral nervous system. Some key points:
- Up to 50% of HIV patients experience clinically apparent neurological disease. Common manifestations involve the brain, meninges, spinal cord, peripheral nerves, and muscles.
- Direct effects of HIV include infection of cells like macrophages, monocytes, microglia, and possibly astrocytes. Indirect effects include opportunistic infections and neoplasms.
- Common CNS manifestations include HIV encephalopathy/dementia, space-occupying lesions, encephalitis, and stroke-like syndromes. Common peripheral
Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Dandy–Walker malformation (DWM) encompasses cystic dilatation of the fourth ventricle, complete or partial agenesis of cerebella vermis and enlarged posterior fossa while Dandy–Walker variant (DWV) comprises cystic posterior mass with variable hypoplasia of the cerebella vermis and no enlargement of the posterior fossa.
Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection that targets cells that make myelin--the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses. The disease is rare and occurs in patients undergoing chronic corticosteroid or immunosuppressive therapy for organ transplant, or individuals with cancer (such as Hodgkin’s disease or lymphoma). Individuals with autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus -- some of whom are treated with biological therapies that allow JC virus reactivation -- are at risk for PML as well. PML is most common among individuals with HIV-1 infection / acquired immune deficiency syndrome (AIDS). Currently, the best available therapy is reversal of the immune-deficient state, since there are no effective drugs that block virus infection without toxicity. Reversal may be achieved by using plasma exchange to accelerate the removal of the therapeutic agents that put patients at risk for PML. In the case of HIV-associated PML, immediately beginning anti-retroviral therapy will benefit most individuals. Several new drugs that laboratory tests found effective against infection are being used in PML patients with special permission of the U.S. Food and Drug Administration. Hexadecyloxypropyl-Cidofovir (CMX001) is currently being studied as a treatment option for JVC because of its ability to suppress JVC by inhibiting viral DNA replication.
In general, PML has a mortality rate of 30-50 percent in the first few months following diagnosis but depends on the severity of the underlying disease and treatment received. Those who survive PML can be left with severe neurological disabilities.
Dandy–Walker malformation (DWM) encompasses cystic dilatation of the fourth ventricle, complete or partial agenesis of cerebella vermis and enlarged posterior fossa while Dandy–Walker variant (DWV) comprises cystic posterior mass with variable hypoplasia of the cerebella vermis and no enlargement of the posterior fossa.
Meningitis is an inflammation (swelling) of the protective membranes covering the brain and spinal cord. A bacterial or viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling. However, injuries, cancer, certain drugs, and other types of infections also can cause meningitis.
Meningitis is a severe CNS pathology and early and appropriate intervention is needed to prevent adverse outcome including mortality and long term complications. This presentation focuses on the different types of meningitis and the appropriate management options
The basics of autoregulation of Gloemrular filtration rate. This ppt deals with basic renal physiology, tubuloglomerular feedback, myogenic reflex, juxtaglomerular apparatus and renin angiotensin aldosterone system in brief. P.S.- The ppt has animations so kindly view in slide/presentation mode
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
How to Give Better Lectures: Some Tips for Doctors
Neurological manifestations of HIV
1. Neurological Manifestations
of
Human Immunodeficiency
Virus
Presenter - Dr.Garima Aggarwal
Moderator - Dr (Brig) Rajesh Kakkar
Dr.Manish Mittal
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. NEUROPATHOGENESIS
Nervous System effects of HIV infection
DIRECT INDIRECT
HIV virus and its products Oppurtunistic infections
HIV associated Neoplasms
Cells affected by HIV -
Perivascular Macrophages
Monocytes from blood
Microglial cells
?Astrocytes
5. CLASSIFICATION OF NEUROLOGICAL MANIFESTATIONS
OF HIV
HIV 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
7. • HIV Encephalopathy/ ADC
• Progressive Multifocal Leuco-
DEMENTIA Encephalopathy
• Tuberculosis
• Neurosyphilis
B • Lymphoma
R • Abscesses
Tuberculosis
Listeria
A Nocardia
E.Coli
I • Infective Granulomas Toxoplasma
N SPACE Aspergillus
OCCUPYING Candida
Cryptococcus
LESIONS
• Neoplastic Primary CNS Lymphoma
Secondary Metastasis
Metastatic Kaposi’s Sarcoma
Glioma
• Others
PMLE, Varicella Zoster, CMV
8. • CMV Encephalitis
• PMLE
• HSV , VZV
ENCEPHALITIS • Toxoplasma Encephalitis
• Aspergillus encephalitis
B •
•
Metabolic Encephalitis
IRIS
R
I
A • Granulomatous Angitis – AIDS associated
• Infectious Vasculitis – Tb, Neurosyphilis,
S
C
I Aspergillus, Mucor
• Varicella Zoster Virus Vasculitis
H
E
• Bacterial Endocarditis, non bacterial thrombotic
N 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.
10. M • HIV Seroconversion Illness-
Aseptic meningitis
E ACUTE • Pneumococcal, Meningococcal
N • E.Coli
• Klebsiella
I • Listeria
N
G • Mycobacterium tuberculosis
• Mycobacterium Avium complex
I • Cryptococcus
• Candida
T CHRONIC
• Syphilis
I • Nocardia
• Metastatic Meningitis -
S Lymphoma
12. M HIV associated • Vacoular Myelopathy
Y
E • CMV Myelopathy
• Varicella Zoster Virus
L INFECTIONS • Herpes Simplex Virus
• HTLV 1 and 2
O • Neurosyphilis
P
NEOPLASTIC • Lymphoma/metastasis associated
A Myelopathy
T
H METABOLIC • Vitamin B 12 Deficiency
Y
16. • HIV Polymyositis
M • CMV Polymyositis
Y INFECTION • Pyomyositis
• AIDS cachexia- HIV associated
O Wasting Syndrome
P
A
T
• ZIDOVUDINE
H DRUG INDUCED • Others especially NRTIS
Y
18. ASEPTIC HIV MENINGITIS
10-15% of patients with Acute HIV Seroconversion illness present
with meningtis
PATHPHYSIOLOGY – Immune mediated illness
CLINICAL FEATURES
Headache – severe and protracted, isolated persistant headache
Signs of meningeal irritation – nausea, vomiting, photophobia
Acute Seroconversion illness – Flu like febrile illness
Preserved alertness and cognition
May be associated with features of Encephalitis
Cranial nerve Involvement may be seen – CN VII, rarely V and/or VIII
It is a diagnosis of exclusion.
19. ASEPTIC MENINGITIS continued
INVESTIGATIONS
1. 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 IgG
3. Serum P 24 capture assay, HIV RNA level
TREATMENT
No specific therapy is needed.
Resolves in 2-4 months without treatment.
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
Dysfunction
HIV 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. HIV ENCEPHALOPATHY continued
CLINICAL FEATURES
Cognitive impairment – Forgetfulness
Decreased Attention and Concentration
Inability to perform complex task
Decreased Sexual drive and disrupted Sleep
Mild mania and Agitation
Motor Dysfunction- Poor balance
Gait incoordination- slow and rigid gait
Slowness of movements
Postural tremors
Choreoform movements, myoclonic jerks
Vegetative state- Bowel and Bladder incontinence
Unable to Ambulate
lying in bed mute with vacant stare
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 Normal
STAGE 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. INVESTIGATIONS – testing done only to exclude other diagnosis
1. Neuropsychological testing – MMSE
It 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, Beta2MG
The practical utility of special CSF testing is uncertain
No absolute correlation exists between CSF HIV burden and disease severity
24.
25. 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.
26. 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
27. INVESTIGATIONS
1. CT/MRI – Hydrocephalus
Complications of
Gelatinous pseudocysts Cryptoccal
Cryptococcomas meningitis
only nonspecific Cerebral Atrophy
2. 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
28. CT brain showing -
1.Gelatinous
Pseudocyst
( formed by
confluence of dilated
perivascular spaces).
2.Sites: Basal
ganglia, cerebral
cortex, cerebellum
and midbrain.
No contrast
enhancement
MRI: Cyst are of CSF
intensity
29. 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 months
Maintainence 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, Ventriculostomy
Acute mortality approaches 30% and is related to inceased ICP
30. TOXOPLASMOSIS of the BRAIN
Associaterd with CD4+T cell count < 100cells/micr.l
Most commmon cause of focal intracranial masses in patients with
AIDS
PATHOGENESIS
It 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
31. INVESTIGATIONS
1. CT / MRI – ‘Multiple lesions in Multiple Locations’
Ring Encancing Lesions – inflammation and central
necrosis
2. 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
34. 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.l
Prophylaxis – HIV ,CD4+Tcell count <100c/mi.l, IgG toxoplasma +ve
Primary Prevention – HIV , but seronegative for toxoplasma
35. PROGRESSIVE MULTIFOCAL LEUCOENCEPHALOPATHY
It is a late manifestation, seen in 4% of patients with AIDS
PATHOGENESIS
Caused by the JC virus, DNA containing HPV. Only known complication
Approx 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
36. INVESTIGATIONS
1. CT / MRI – Multiple nonenhancing white matter lesions,
may coalesce, predilection for occipital and parietal.
MRI – decreased signal intensity on T1
- Hyperintensity on T2
2. 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
37. FLAIR Images Showing
Progression of Progressive
Multifocal Leukoencephalopathy
a) Multifocal, high-signal-
intensity lesions (arrow) in the
right hemisphere of a patient The
CSF was positive for JC virus.
b) Contrast
enhancement is not evident
(arrow).
c ) 6 weeks later, progression
of the white matter lesions
(arrow) shows involvement of the
uncinate fibers.
d )Patchy enhancement with
gadolinium
(arrow) is noted (predominantly
in the right hemisphere
38. T2 flair MRI brain shows White matter hyperintensity of subcortical U fibers, splenium of
corpus callosum in posterior cerebral hemisphere
No contrast enhancement
No mass effect
Common sites: temporal and occipital white matter, Subinsular region, corpus callosum
and subcortical U fibers
39. TREATMENT
No specific therapy available for PMLE
Improved survival has been seen with HAART
HIV with PMLE
without HAART with HAART
Mean Survival- 3 – 6 months around 2.5 years (>7years*)
Patients on HAART may show paradoxical worsening due to IRIS
Only 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
40. PRIMARY CNS LYMPHOMA
Complicate the course of AIDS in upto 5% of patients.
PATHOGENESIS
PCNSL of B cell origin are considered oppurtunistic neoplasms.
CLINICAL FEATURES
Similar 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
41. INVESTIGATIONS
1. 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 rare
2. CSF – unhelpful
- Monoclonal B lymphocytes by flowcytometry Corroborative
evidence on
- CSF – EBV virus DNA amplification PCNSL
3. BRAIN BIOPSY – definitve diagnosis
- After a failed therapeutic trial for Toxoplasmosis
4. SPECT SCAN – may be useful.
42. 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
43. 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.
44. 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
45. VACUOLAR MYELOPATHY VITAMIN B12- sacd
S. Vitamin B12 levels are Normal Decreased
Usually 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.
46. INVESTIGATION nonspecific , to exclude other etiologies
1. MRI SPINE – Cord swelling wtith intramedullary enhancement
- T2 signal changes
2. 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.
47. Sagittal T2-weighted
images of the cervical
C2 spine-
Iintramedullary
signal
increased signal on T2
C5 enhancement extending from C2
though approximately
C5.
The axial T2 image-
Abnormal signal to be
symmetric within the
posterior columns of the
cord.
48. 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.
NEUROPATHY
Distal Sensory CMV assoc. NRTI assoc. TOXIC
AIDP and CIDP
PN POLYRADICULOPATHY NEUROPATHY
49. 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
51. References
1. Neurology in Clinical Practice – 3rd edition
(Bradley, Daroff, Fenchal)
2. Adams and Victor’s Principles of Neurology- 9th
edition
3. Harrison’s principles of Internal Medicine – 17th
edition
4. Textbook of neurology- Dounghey
5. NACO guidelines for management of AIDS- 2010
6.WHO guidelines for HIV/AIDS
7. World Wide Web