MSC Neuro 25 p2
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Caused by tick-borne encephalitis virus (TBEV), a neurotropic virus transmitted primarily via bites of infected ixodid ticks.
TBEV is maintained in vertebrate hosts like rodents and small ungulates; transmission occurs during tick's feeding period, mostly in spring and summer.
Transmission routes: tick bite (skin entry), sometimes ingestion of unpasteurized milk from infected animals.
Pathogenesis:
Virus invades nervous system via hematogenous spread or along peripheral nerves ("neuroprobasia").
Infects motor neurons in spinal cord (esp. cervical enlargement) and brain structures.
Initial viral replication in peripheral tissues, then CNS invasion in biphasic illness.
Clinical Forms:
1.Asymptomatic Carriage: Especially in endemic inhabitants with prior immunity.
2.Abortive Form: Mild systemic symptoms resembling influenza.
3.Nerve Paralytic Form: Damage to peripheral nerves causing polyradiculoneuritis; sensory loss, distal limb weakness, neuropathic pain.
4.Meningeal Form: Inflammation of meninges presenting with fever, headache, vomiting, early meningeal signs.
5.Encephalitic Form: Involvement of brain tissue; focal neurologic deficits, motor paralysis, cranial nerve palsies, altered consciousness, seizures.
Symptoms:
Biphasic illness: initial fever, malaise, headache; after improvement, neurological symptoms arise.
Early: fever (up to 40°C), headache, vomiting, hyperesthesia, photophobia.
Neurologic: meningismus, cranial nerve involvement (III, VI, VII), weakness or paralysis, altered mental status.
Severe cases may have seizures, coma.
Diagnosis:
Clinical assessment and history, including tick exposure and season.
Serology: detection ofTBEV-specific IgM and IgG antibodies in serum or CSF.
PCR sometimes used but less sensitive in late phase.
Neuroimaging (MRI) may show focal lesions.
CSF analysis: elevated protein, lymphocytic pleocytosis, elevated pressure.
Treatment:
No specific antiviral therapy.
Supportive care in hospital: hydration, symptom control.
Antiviral agents (e.g., ribonucleases) have limited use.
Prevent secondary infections (e.g., antibiotics for pneumonia).
Corticosteroids to control inflammation in some cases.
ICU care for severe neurological impairment, including ventilation support if needed.
Prevention:
Avoidance of tick exposure via protective clothing, repellents.
Vaccination available in endemic areas; recommended for at-risk populations (foresters, outdoor workers).
Post-exposure prophylaxis: no effective therapy; immediate tick removal essential.
Public health measures include education and surveillance.
Herpes Simplex Encephalitis (HSE):
Etiology
Caused primarily by Herpes Simplex VirusType 1 (HSV-1) (less frequently HSV-2).
HSV-1 typically affects the frontotemporal lobes.
Often results from reactivation of latent virus or primary infection.
Pathogenesis
CNS infection after viral entry and replication in brain tissue.
Viral infection causes necrosis and inflammation of neurons (necrotizing encephalitis).
Extent of brain damage depends on viral replication and host immune response.
Clinical Features
Prodromal phase: Fever, malaise, headache.
Acute phase:
Altered mental status (confusion, delirium).
Focal neurological signs (hemiparesis, aphasia, cranial nerve palsies).
Seizures (sometimes focal).
Behavioral and personality changes.
Possible hallucinations, psychosis.
In infants: lethargy, irritability, seizures, poor feeding.
Reflexes may be affected; possible autonomic dysfunction.
Diagnosis
CSF analysis: Mildly elevated opening pressure; lymphocytic pleocytosis; elevated protein; normal or slightly decreased glucose.
PCR testing of CSF: gold standard for HSV DNAdetection.
MRI: abnormal signals in temporal lobes and other affected brain areas.
EEG: focal slowing or epileptiform activity.
Brain biopsy: rarely needed; used if diagnosis uncertain.
Treatment
Antiviral therapy: IV Acyclovir (10-15 mg/kg every 8 hours) for 14-21 days.
Adjunct corticosteroids may reduce inflammation.
Supportive care: seizure management, airway protection, hydration.
Prognosis improved significantly with early treatment but sequelae common (cognitive deficits, epilepsy).
Prevention
No specific vaccine; standard hygiene and preventive measures for HSV infection.
Research ongoing on antivirals and immunomodulators.
12.Neurosyphilis. Clinical forms. Early syphilitic meningitis. Dryness of the spinal cord (Transverse Myelitis). Clinic, diagnosis, and treatment.
Neurosyphilis: Clinical Forms, Diagnosis, andTreatment
Clinical Forms:
1.Early Neurosyphilis:
Occurs within the first few years of infection.
Manifests primarily as meningitis, meningovascular syphilis, or involvement of peripheral nerves (neuritis, polyneuritis).
Symptoms include headache, fever, stiff neck, vomiting, neurological signs (cranial nerve palsies), meningeal irritation.
2.Tabes Dorsalis ("Dry Spinal Cord"):
Typically occurs years to decades after initial infection (latent period of 5–50 years).
Pathological changes affect the posterior roots and columns of the spinal cord.
Clinical features:
Severe, shooting radicular pains.
Loss of deep tendon reflexes.
Sensory ataxia leading to unsteady gait.
Bladder disturbances, impotence.
Argyll Robertson pupil (small, irregular pupils unreactive to light but reactive to accommodation).
Pseudoparetic phenomena such as muscle weakness may be present.
Other signs include Charcot joints, trophic ulcers.
3.Other Late Forms:
General paresis (chronic meningoencephalitis).
Gumma formation causing focal neurological deficits.
Diagnosis:
Based on clinical presentation, patient history, serological testing (RPR, VDRL, FTAABS).
CSF analysis:
Pleocytosis (increased lymphocytes).
Elevated protein.
Positive CSF VDRLor FTAtests.
Neuroimaging:
MRI or CT may show nonspecific findings such as meningeal enhancement, infarcts, atrophy.
Must differentiate from other neurological diseases (e.g., sarcoidosis, vasculitis).
Treatment:
Penicillin G is the treatment of choice:
High-dose IVpenicillin for 10–14 days to achieve adequate CNS levels.
Alternative: Ceftriaxone in penicillin-allergic patients.
Pre-treatment with corticosteroids may be given to reduce Jarisch-Herxheimer reaction (fever, symptoms worsening).
Monitor treatment response by repeated CSF analyses at intervals for up to 2 years.
If CSF abnormalities persist or symptoms worsen, retreatment is recommended.
Symptomatic and rehabilitative therapies for neurological deficits.
Early recognition and treatment improve prognosis and reduce complications.
Transverse Myelitis (TM):
1.Definition
TM is an inflammatory disorder of the spinal cord causing blockade of nerve impulse transmission both ascending and descending across affected segments.
2.Etiology and Pathogenesis
Often idiopathic or post-infectious (30-40% cases after viral infections).
Infectious agents: viruses (herpes simplex, varicella zoster, enteroviruses, HIV, Epstein-Barr), bacteria (syphilis, tuberculosis, Lyme), parasites.
Autoimmune-mediated attack on spinal cord myelin and neurons.
Could be manifestation of systemic autoimmune diseases (SLE, Sjogren's), or part of demyelinating diseases (MS, neuromyelitis optica).
Pathological changes include demyelination, inflammation, edema, necrosis in spinal cord.
3.Clinical Features and Syndromology
Sudden onset (hours to days) of pain (back, radicular), weakness starting in legs and progressing upwards.
Sensory disturbances: numbness, tingling, sometimes sensory level on body.
Possible bilateral motor weakness or paralysis (paraplegia or quadriplegia depending on level).
Autonomic dysfunction: urinary retention/incontinence, bowel dysfunction, sexual dysfunction.
Depending on level of lesion, severity varies.
Signs include sensory level, reflex changes, positive Babinski, spasticity in chronic phases.
4.Complications
Permanent paralysis or paresis.
Bladder and bowel dysfunction.
Pain syndromes.
Secondary infections, pressure sores due to immobility.
5.Diagnosis
Clinical presentation and neurological exam.
MRI: important for detecting spinal cord inflammation and lesion extent.
CSF analysis: pleocytosis (mainly lymphocytes), elevated protein.
Blood tests: infection markers, autoimmune panels.
Exclusion of mimics (compressive myelopathy, vascular cord lesions).
6.Treatment
High-dose intravenous corticosteroids (e.g., methylprednisolone) for 3-5 days.
Plasma exchange or IVimmunoglobulin in steroid-refractory cases.
Symptomatic management: pain control, spasticity drugs, bladder and bowel care.
Physical therapy and rehabilitation for motor recovery.
Treat underlying infection or autoimmune disease if identified.
13. Brain abscess, spinal epidural abscess.
Brain Abscess
Definition:
Localized pus collection within brain tissue, most commonly intracerebral; can be epidural or subdural.
Etiology:
Common pathogens: Streptococcus, Staphylococcus aureus, Pneumococcus, Neisseria meningitidis; also E. coli, Proteus, and mixed flora.
Types:
1.Contact abscess: From adjacent infections such as mastoiditis, otitis media, sinusitis, dental infections. Spread via bone or venous sinuses to brain; common in temporal, frontal lobes.
2.Metastatic abscess: From septic emboli, often multiple, commonly from lung infections, endocarditis, intra-abdominal abscesses.
3.Traumatic abscess: Post head injury or neurosurgical procedures with contamination.
Pathogenesis:
Inflammation and necrosis leading to purulent lesion; encapsulation occurs over weeks forming a fibrous capsule.
Clinical Features:
Fever, chills, headache (progressively worsening), nausea, vomiting.
Neurological deficits depending on abscess location (focal signs, seizures).
Signs of increased intracranial pressure (papilledema, drowsiness).
Possible mental changes.
Diagnosis:
MRI with contrast or CT scan confirms abscess location and size.
Blood tests: leukocytosis, elevated ESR.
Microbiological studies from abscess aspiration or blood cultures. Treatment:
Empiric intravenous antibiotics targeting likely organisms: e.g., ceftriaxone + metronidazole, vancomycin if staphylococcal suspected.
Surgical drainage via stereotactic aspiration or craniotomy if large or not responding to antibiotics alone.
Supportive care including seizure control, intracranial pressure management. Prognosis:
High morbidity and mortality if untreated or delayed diagnosis.
Spinal Epidural Abscess
Definition:
Collection of pus in the epidural space of spinal canal causing compression of spinal cord and nerve roots.
Etiology:
Staphylococci most common; others include gram-negative bacteria.
Risk factors: skin infections, spinal trauma, intravenous drug use, immunosuppression, surgical interventions.
Infection spreads by direct extension or hematogenous route. Clinical Features:
Back pain localized to affected spine level, fever.
Radicular pain developing after few days; sensory disturbances below lesion.
Progressive weakness or paralysis of limbs, bladder and bowel dysfunction.
Signs of spinal cord compression.
Diagnosis:
MRI is gold standard for detection.
Blood tests show leukocytosis, elevated ESR.
Spinal radiographs may show vertebral osteomyelitis. Treatment:
Prompt parenteral antibiotics.
Surgical decompression and drainage if neurological deficits progress or not improving with antibiotics.
Supportive care and rehabilitation.
14, 15. Multiple sclerosis. Etiology, pathogenesis, clinic,Types of course, diagnosis, treatment.
Multiple Sclerosis (MS)
Classification of Multiple Sclerosis
1.Clinically Isolated Syndrome (CIS):
First episode of neurologic symptoms lasting ≥24 hours caused by demyelination; may or may not progress to MS.
2.Relapsing-Remitting MS (RRMS):
Characterized by clearly defined attacks (relapses) followed by periods of partial or complete recovery (remission).Accounts for ~85% of cases at onset.
3.Secondary Progressive MS (SPMS):
Initially starts as RRMS; eventually transitions to steady worsening with or without relapses.
4.Primary Progressive MS (PPMS):
Steady progression of neurologic disability from onset without remission; ~10-15% of patients.
5.Progressive-Relapsing MS (PRMS):
Progressive disease from onset with acute relapses.
6.Other categories:
Benign MS (minimal disability after long duration)
Malignant MS (rapid progression with early disability)
Radiologically Isolated Syndrome (RIS)
Etiology
Multifactorial: Genetic predisposition (e.g., HLA-DRB1*15 allele), environmental factors (viral infections like EBV), smoking, vitamin D deficiency.
Autoimmune mediated attack on CNS myelin involvingT cells, B cells, and macrophages.
Pathogenesis
Demyelination of CNS neurons leads to conduction block and neuronal loss.
Initial inflammation causes reversible demyelination; repeated attacks lead to axonal loss and irreversible damage.
Formation of plaques (sclerosis) predominantly in periventricular white matter, brainstem, cerebellum, and spinal cord.
Clinical Features
Varied neurological symptoms reflecting CNS demyelination:
Motor: Pyramidal weakness, spasticity
Sensory: Numbness, paresthesias
Visual: Optic neuritis, diplopia
Coordination: Ataxia, tremor
Brainstem: Cranial nerve palsies, nystagmus
Sphincter: Urinary dysfunction
Cognitive/Psych: Cognitive decline, emotional lability
Characteristic signs: Uthoff’s phenomenon (symptom worsening with heat), Lhermitte’s sign (electric shock sensations on neck flexion).
Disease course varies widely.
Diagnostics
Clinical criteria including dissemination in time and space.
MRI: T2/FLAIR hyperintense lesions in characteristic locations.
CSF analysis: Oligoclonal bands, elevated IgG index.
Evoked potentials: delayed conduction.
Exclusion of mimics.
Treatment
No cure; aim to reduce relapse frequency and progression.
Acute exacerbation: High-dose corticosteroids (e.g., methylprednisolone).
Disease-modifying therapies (DMTs): Interferon-beta, glatiramer acetate, natalizumab, fingolimod, ocrelizumab, among others.
Symptomatic management: spasticity, bladder dysfunction, fatigue.
Physical and occupational therapy for rehabilitation.
16.Parkinson's disease: Etiology, pathogenesis, clinical forms.
Parkinson's Disease (PD):
Etiology