Neuro 2 - Stroke & Meningitis

• Non contrast CT head:
• Normal (in majority cases).
• to rule out haemorrhagic stroke

• Thrombolysis can cause increased bleeding risk.

• Hyperdense MCA sign
• Early clot in MCA appears hyperdense
• uncommon
• Later → hypodensity.

• Blackish hypodensity
• which develops over time.
• Ischemic damage

• Acute stroke
1. White → s/o Acute hemorrhage/clot
2. Well-defined hypodense infarct in MCA region.
3. Hypodensity in thalamus: Lacunar infarct
• Charcot's artery/ LS branch of MCA

• White artery (MCA) → Hyperdense artery sign → Acute thrombus

• Loss of insular ribbon:

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• In MCA stroke → insular cortex becomes oedematous first
• because of its closest proximity to Lateral sulcus





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• DWI: Restricted diffusion S/O acute infarct.



• Chronic infarct: No restricted diffusion (due to CSF).

Moya Moya disease

 

• On DSA, ICA is shown.

• Due to ICA stenosis and collateral development.
• Black narrowed vessels are seen.
• Contrast appears as a puff of smoke.

• Prehospital: Call ahead, activate Code stroke.

Onset <6 h: (“Last seen well” is used for calculation)

• CT: No hemorrhage.

• IV PA eligible?
• If yes: Give IV PA.
• Alteplase → Bolus f/b infusion
• At CT scan: Tenecteplase → Single bolus
• If Not: Perform CT angiography
• Detects Emergent large vessel occlusion (ELVO).
• ICA or M 1-2 of MCA or Basilary Artery occlusion?
• If ELVO present → do CT Perfusion
• checks penumbra vs ischemic core mismatch.
• helps pick up penumbra.
• Viable ischemic areas that can be saved.
• If yes: Consider Mechanical Thrombectomy → MERCI

Onset 6–24 h:

• CT: No hemorrhage.

• CTA/CTP: Favorable perfusion?
• If yes: Thrombectomy → MERCI

Role of MRI (DWI)

• Most sensitive than NCCT for early infarct.

• Not preferred (time, cost, limited availability).

Brain Areas and Blood Supply

Applied Aspect

• ACA stroke:
• Causes C/L LL paralysis
• Incontinence.

ACA stroke

• Paracentral Lobule
• Urinary incontinence
• C/L paralysis and sensory loss: lower limb
• Highest centre for micturition & defecation

• Personality changes

• Anton Syndrome
• Denial of blindness + Confabulation

• Note: Middle cerebral artery does not form the Circle of Willis.

• Labyrinthine artery: Branch of AICA

• Ophthalmic artery: 1st branch of ICA

• Internal carotid: main brain supply.

• Posterior cerebral artery: From basilar artery.

Lumbar puncture

• L3-L4 or L4-L5;
• choose widest space.

Indications of CT before Lumbar Puncture: FAILS

• Focal neurological deficit

• Altered mental status

• Immuno-compromised

• Lesion

• Seizure

• Papilledema

Needles

• Dura cutting:
• Increased Post Dural Puncture Headache (PDPH).
• Pointed edge
• Technically easier.
• Examples: Quincke (most common).
• Mnemonic: Kuttunnath → quincke

• Dura splitting:
• Decreased PDPH.
• less traumatic
• Technically difficult.
• Examples: Whitacre, Sprotte
• Mnemonic: Wisely (Whitacre Sprotte) Split

• Steps
• Advance needle cephalad (bevel up).

• After CSF appears
• re-insert stylet halfway to prevent herniation.

CSF tubes

Clinical features

• Fever.

• Headache.

• Seizures.

• Nuchal rigidity.

• Vomiting (if ICP is raised).

• Sleepiness, irritability.

• Delirium (if undiagnosed).

• Focal neurological signs may be seen.

• Altered sensorium/encephalopathy.

• Anorexia.

• Infant:
• Non-specific features:
• Poor feeding.
• Lethargy.
• Irritability with shrill cry.
• Petechiae.
• Purpura.

• Older children (12-18 months of age:):
• headache.
• Photophobia.
• Myalgia & arthralgia.
• Blurring of vision.
• Diplopia.

Signs of meningeal irritation

• Neck rigidity.

• Meningeal signs:
• Kernig's sign,
• Brudzinski' sign.

• Younger infants:
• Tense Bulging fontanelle.
• Widening of sutures.

Examination

• AMOSS sign/Tripod sign.

• Nuchal rigidity:
• Ask patient to touch chin to chest.

• Kernig sign:
• Mnemonic: Knee extension → Kernig
• Supine, extend leg at knee (pain in hamstrings or back).

• Brudzinski sign
• Neck flexion
• passive flexion of hip and knee,

• Jolt accentuation test:
• Turn head side-to-side rapidly; increases pain.
• False positives in headache patients.

Fundus examination:

• Papilledema.

Workup

• Blood culture for hematogenous spread.

• Start empirical antibiotics within 1 hour.
• Does not affect CSF findings.

• NCCT done before LP
• exclude raised ICP/midline shift.

Treatment:

• Isolate Till 24 hours after starting antibiotics

• Prompt initiation of empirical antibiotics.

• IV 3rd gen. cephalosporin (ceftriaxone)
• Child: 7-10 days
• Neonate: 3 weeks
• No response in 48 hours
• Add vancomycin

• Steroids Along with first dose of IV antibiotics.
• DOC : Dexamethasone x 2 days
• goal : ↓↓ incidence of SNHL.

• Duration
• Streptococcal meningitis:
• 7–10 days
• Gram-negative meningitis (excluding neonatal cases):
• 3 weeks
• Staphylococcal meningitis:
• 3 weeks
• Meningococcal meningitis:
• 7 days
• Prophylaxis of Meningococcal meningitis
• Ceftriaxone
• Safe in
• pregnancy
• In childrens
• Rifampicin
• Safe in childrens
• For 2 days
• Not in pregnancy
• Ciprofloxacin
• Not in
• pregnancy
• In childrens

Complication

• SNHL in Children

• Often follows S. pneumoniae-associated meningitis

• Investigation: Brain evoked response audiometry (BERA)

CASE

• Immunocompromised history ⇒
• Cryptococcosis

CASE

• Q. With immunocompromised history ⇒
• Pneumococcus if
• Diagnosis
1. Gram-positive diplococcus.
2. India ink positive.

• Treat with antibiotics.

CASE

• CSF: Cobweb coagulum.

• Diagnosis: Tubercular meningitis.

• Weeks-long history, gradual onset, hydrocephalus may occur in kids.

• CSF:
• Lymphocytic pleocytosis,
• low sugar,
• V. high protein.

• Bacterial meningitis:
• CSF
• Marked sugar drop (hypoglycorrhachia).
• Neutrophils seen.

• CSF protein:
• Normal:
• 15–45 mg%,
• in TBM:
• 10–20 × norm.

• Normal CSF sugar:
• >2/3 blood sugar.

CSF findings summary table

• Routes: Important
1. Pork
• larvae → intestinal tapeworm.
2. Vegetables on contaminated soil (like cabbage)
• eggs → neurocysticercosis.

• Cysticercosis:
• Rice-grain calcification (dead larvae).
• Alternative: Steroids, Praziquantel.

Neurocysticercosis

• Soli sir affect brain → he is sole cause (sub kuch infective - egg and larvae) → Nakshathram enni (starry sky)
• he was Para (Parenchyma brain)
• solium - systi sercus sellulose → inside the cell

• Cysticercus cellulosae:
• zig-zag tube, hooklets, suckers, convoluted tube-like structure

• Scolex in brain.

• M/C site : Brain parenchyma

• M/C presentation: Seizures

• Imaging: Gadolinium MRI preferred.
• Starry sky appearance

• Drugs: Steroids f/b Albendazole (DOC)
• ↓ inflammation d/t dying larvae

Clinical features

• Low socioeconomic status.

• Multiple focal seizures.
• Vasogenic cerebral oedema can cause focal seizures.

General exam

• Multiple subcutaneous lumps/bumps.

First:

• LP (guarded)
• CSF immunoblot for NCC antigen
• (NOTE: CSF ELISA is for cryptococcus)

NCCT

• Starry sky appearance d/t calcification
• But not early on CT.







• Cyst with a dot inside (scolex).
• End stage: can be calcified.
• Starry sky appearance.
• Can spread to muscles.
• Rice grain calcification.
• Can cause hydrocephalus.

Imaging:

• Gd-MRI.

• Vasogenic cerebral edema

Stages of Lesion in Radiology

Treatment of NCC

1. Start dexamethasone (48h) to control edema.

2. Albendazole
• not started first because
• prevents inflammatory reaction
• ↑ seizures

3. CBZ/Lamotrigine: For seizures.

MR Spectroscopy

• Creates a graph of chemical metabolites.

Condition	Maximum Peak
Normal brain	NAA
Tumor	Choline
Tuberculosis	Single lipid peak + basal exudates
Neurocysticercosis	Multiple amino acid peaks.

Comparison Table

• New world
• Pigeon droppings + Immunodeficient people
• Easily treatable
• + Negative (India ink) Music (Mucicarmine)

• Old world → Gatti
• Trees (eucalyptus tree) with leaf (LFA) and latex
• immunocompetent + Immunodeficient people
• Tropical climate
• difficult to treat diseases

Clinical features

• Fever, headache, photophobia, vomiting, nuchal rigidity.

• Seen in immunocompromised,
• e.g. AIDS truck driver.

Workup

• First:
• Blood culture,
• start empiric antibiotics in 1 hr.

• Empiric:
• Ceftriaxone + vancomycin (no cryptococcal coverage).

• NCCT:
• Check raised ICP.

• Brain biopsy:
• In dead
• Mucicarmine

• CD4 <100 needed for disease.

LP:

• CSF cell counts.
• Lymphocytic pleocytosis.

• Slightly reduced sugar, high protein (norm: 15–45 mg%)

• Gram: No organism.

• CSF ELISA (Ag) is IOC.

• India ink / Nigrosin:
• Positive > Negative (not reliable).

Culture

• Agar: Bird seed / Niger seed agar

• Colour: Brownish due to Phenol Oxidase / Laccase

Confirmatory Test

• Lateral flow assay > latex agglutination
• Lateral flow assay ⇒ cryptococcal antigen
• Serum/plasma/CSF.
• More sensitive and specific
• Latex agglutination ⇒ Glucuronoxylomannan

• Cryptococcus found in pigeon droppings, dust.
• Healthy:
• No CNS disease due to immunity.
• Immunosuppressed:
• Lung → brain (via blood)

Treatment

• Amphotericin B >> (+) flucytosine
• Not LAMB (For Kala azar)

• Prevention/Maintenance
• Fluconazole (when CD4 < 100)

AMB

• Side effects
• Nephrotoxic
• Liposomal AMB is less nephrotoxic.
• (Cryptococcal, Mucor uses AMP)
• Infusion reaction
• RTA type 1
• Hypokalemia
• BM suppression

• GBS is an 
• acute onset (≤4 weeks)
• bilateral symmetrical
• inflammatory
• autoimmune polyradiculoneuropathy.

• Autoimmune Demyelination of peripheral nervous system.

• Ascending, symmetrical, flaccid paralysis.

• 7th cranial nerve is most commonly involved

• Bladder and bowel spared (if involved → transverse myelitis)

• GBS is usually post-infectious (2-3 weeks).
• A/w Campylobacter

• AIDP is most common GBS.

• Antibody: Anti GM1 Antibody.
• NOTE:
• Miller Fisher: Anti GQ1 Antibody.
• Mnemonic: Fish vangan Que nikkanam

• Brighton criteria for diagnosis.
• NOTE: Revised McDonald criteria for Multiple sclerosis.

Pathophysiology

• IgG Antibodies → Bind to Myelin/Axons → Activates complement → Macrophage invasion → Vesicular degeneration

Inciting Factors/Triggers

• Gastroenteritis/URTI (Past 4 weeks):
• Present in 60-70% of GBS cases.

• Campylobacter jejuni (Most common trigger)
• Molecular mimicry implicated.

• CMV (Cytomegalovirus)

• EBV (Epstein-Barr Virus)

• Mycoplasma

• Hep A/B

• HIV

• Zika virus

• Vaccination associated.

• C. jejuni also A/w
• IPSID- Immunoproliferative Small Intestinal Disease/Lymphoma

Features:

• Earliest sign: Distal areflexia.

• Bilateral ascending symmetrical flaccid paralysis.
• Maximum severity of 2 weeks after initial onset

• B/L atonic areflexic paraparesis (Proximal > distal) of lower limbs.

• Equal paralysis of both legs
• quadriplegia

• Neuropathic pain, particularly in the legs
• Large fibre (Aα) sensory loss.

• Truncal paralysis
• Cant sit up in the bed

• Cervical demyelination
• respiratory paralysis

• Neck floppiness.

• 7th nerve palsy (facial diplegia) → M/c CN involved

• In severe cases ➔ Respiratory failure ➔ FVC should be done to assess ventilation

Brighton Criteria for GBS

• Bilateral and flaccid limb weakness.

• Decreased/absent deep tendon reflexes in weak limbs.

• Monophasic course;
• onset 12 hours to 28 days.

• No alternative diagnosis for weakness.

• Albumino-cytological dissociation

• Nerve conduction:
• consistent with GBS (latency increased).

Prognosis

• 80% recover.
• Begins 2-4 weeks after progression ceases.

• 4-15% mortality.

Bad Prognostic Factors

• Autonomic Nervous System
• Labile hypertension (Extreme BP fluctuations).
• Postural hypotension (Orthostatic hypotension).
• Arrhythmias.
• Anhidrosis.
• Tachycardia.

Typical Electrodiagnostic Features (NCS)

• Prolonged latency.

• Decreased conduction velocity.

• Conduction block.

• Absent/prolonged F-wave & H-reflex.

• Temporal dispersion.

LP: Albumino-cytological dissociation.

• CSF cells < 50/ml

• CSF protein concentration > 60 mg/dL.

• CSF opening pressure: normal.

• Sugar: normal.

• Color: normal.

Treatment

• DOC: IV Immunoglobulins.

• Plasmapheresis → PLEX (Plasma Exchange) Therapy

• Both therapies equally effective.

• No role for steroids.

DD

• Transverse myelitis vs GBS
• Bladder/bowel involvement.
• Root pain.
• Urinary incontinence.

Comparison Table

• CIDP (Chronic Inflammatory Demyelinating Polyneuropathy):
• Chronic, >8 weeks.

Classification

• All antibodies associated are IgGs.

 

• Kerala:
• Nipah virus (NiV) 2018 caused outbreak.
• Enveloped Non-segmented RNA Virus
• Paramyxovirus

• Causes encephalitis ± ARDS.

• Route: Human-to-human via secretions.

• Clinical: Encephalitis, fever

• Mortality rate: 60 - 80%

• Infection by:
• Reservoir: Fruit Bat genus → Pteropus.
• primary vector
• Bat urine/saliva/feces contaminates date palm sap
• Contaminated fruit eaten by pig → pig to human/pork exported.
• Pigs = amplifiers
• Virus also in patient secretions

• No treatment exists.

• To diagnose: PCR of CSF for Nipah.

• CSF: Monocytes, clefted nuclei (Mollaret cells).

• Variant of aseptic meningitis.

• Virus: HSV-2.
• Causes recurrent aseptic meningitis.

Leading viral encephalitis

• India: Japanese B.

• worldwide: Herpes simplex.