Module 9: Nervous System Flashcards by LENNIE BELLE PORTENTO

This restricts the entry of pathogens into the brain and meninges

Hematogenous spread of organisms
requires spread through at least 2
layers to infect the brain

Blood Brain Barrier

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3 Hematogenous Spread (Bloodborne Invasion) into the CNS?

Growing across (Microbes can grow in the endothelial cells)

Passive (Transported across in intracellular vacuoles)

Carried in infected cells (Infected inflammatory cells)

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This virus may invade Muscle Cells at the Bite Site > Move up the Nerves to the Dorsal Root Ganglia > Spinal Cord > Brain

Rabies and other Lyssaviruses

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This virus may migrate up the nerves
using normal retrograde transport
mechanisms

Herpes viruses

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Inflammation of the Meninges of the brain due to viral etiology.
- (Eg. By Herpes Simplex Virus)

Viral Meningitis

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Inflammation of the Meninges of the Brain
due to Bacterial Etiology.
- (Typically: Neisseria Meningitidis,
Streptococcus Pneumoniae, Hemophilus
Influenzae

Bacterial Meningitis

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Inflammation of the Brain
- (Typically due to Viruses – eg. Herpes
Simplex)

Encephalitis

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Inflammation of the Brain & the Meninges

Meningoencephalitis

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Inflammation of the Spinal Cord > Disrupts
CNS functions liking the brain & limbs.
- Eg. Poliovirus (Poliomyelitis)

Myelitis

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Inflammation of the Brain and Spinal Cord
- Typically Immune-mediated following a viral
infection.
- (Eg. Acute Disseminated Encephalomyelitis
– Following Influenza, enterovirus, measles,
mumps, rubella, varicella zoster, etc.)

Encephalomyelitis

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Encapsulated Pus or Free-Pus in the Brain after an Acute Focal Purulent Infection.
- (Focal Infections include: Otitis Media/Sinusitis)

Brain Abscesses

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Presentation: Meningism:
- *Neck Stiffness
- *Photophobia
- *Headache
- (Fever/Malaise)

MENINGITIS

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How many Samples are taken for CSF Examination? And what types?

3 (Serology, Biochemistry, Bacteriology)

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What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Negative Diplococci
- Usually in Stressed/Crowded
- Severe toxin sequalae > Tissue damage
- Vaccine only for Serotypes A & C (Not B –
Which is the most common)
- Immune System has to Start Again because of Immunogenicity of its capsule

Neisseria Meningitidis

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What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Negative Cocco-bacilli
- Usually in Children / Babies
- Toxin production > Tissue damage
- Vaccine Available (Hib Vaccine)

Hemophilus Influenza

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What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Positive Cocci
- Predisposed Adults
- Neonates

Streptococcus Pneumoniae

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Other Etiologies: Type of Meningitis?
- Escherichia coli
- Group B Streptococci
- High Mortality Rates (35% of cases)

Neonatal Meningitis

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Other Etiologies: Type of Meningitis?
- Mycobacterium tuberculosis
- Acid fast bacilli (Stains with Ziehl Neelsen
stain)
- Patients Typically have a Focus of Infection
Elsewhere

Most of cases are associated with Miliary
(disseminated) Tuberculosis

Tuberculous Meningitis

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Features Suggestive of etiology of Meningitis:

erythematous, petechial / purpuric.
Suggests meningococcus (rarely Pneumococcus or Hemophilus influenzae type b)

Rash

Features Suggestive of etiology of Meningitis:

Basal skull fracture
a. Pneumococcus, H. influenzae, Hemolytic
Strep.
b. (CSF Rhinorrhea refers to the drainage of
Cerebrospinal Fluid through the nose. It is a
sign of Basal Skull Fracture)

CSF rhinorrhea or otorrhea

Mainly Cryptococcus Neoformans
- Typically in Immunosuppressed
- Can be treated with antifungal drugs

Fungal Meningitis

Less Severe than Bacterial
- More Common than bacterial.

(HSV, Mumps, Poliovirus, Enterovirus 71, Japanese encephalitis, HIV)

Viral Meningitis

What virus that causes inflammation to the brain?

The infection progresses back to the
temporal lobe of the brain. 70% mortality rate in untreated patients

Treatment with Acyclovir > ↓Mortality rate

Herpes Simplex Virus

Clinical Feature: Paralysis may extend from a single muscle to virtually every skeletal muscle
- There may be involvement of respiratory
muscles > Lifelong Assisted Ventilation

Poliovirus (Encephalitis)

Advantages: - Easy Administration - Given Orally - Cheap - Induces intestinal local immunity - More Robust Immune Response Disadvantage: - Rarely causes paralysis (1 in 2.5million)

Live Attenuated (Oral Polio Vaccine)

Advantages: - Carries NO risk of Vaccine-Associated Polio Paralysis - Very Robust Immune Response Disadvantage: - Difficult Administration - Has to be injected - Confers little Mucosal Immunity in the Intestinal Tract. - 5 Times more expensive than OPV

Inactivated Polio Vaccine (IPV)

Organism: - Rhabdovirus (A Bat Virus) Transmission: - by the bite of an infected animal - The virus is present in the saliva of the infected animal (Dogs, foxes and other wild species)

Rabies Encephalitis

Sites of Focal Infection that could lead to this infection? o Otitis Media o Sinusitis o Penetrating trauma o Hematogenous dissemination

BRAIN ABSCESS

Etiology: - Alcohol Abuse > Vit B1[Thiamine] Deficiency Clinical Features: - Cortical Atrophy > Impaired Memory (Anterograde & Retrograde) + Confabulation - Mamillary Body Damage > Vision Changes, Nystagmus, Unequal Pupils Cerebellar Atrophy > Ataxia

WERNICKES-KORSAKOFF SYNDROME (Alcoholic Encephalopathy)

Global Degeneration Dementias - (Age-Related (Senile) Dementia - Alzheimer’s - Lewy-Body Dementia - Fronto-Temporal Dementia/Pick’s Disease

DEGENERATIVE DISEASES

Acquired Global Impairment of Intellect, but with no ALOC. Epidemiology: o 5% of >55yrs are demented o 20% of >80yrs are demented o Prevalence Doubles every 5yrs beyond Age:60. o 50% of dementia pts have clinically significant behavioral/psychological symptoms

Dementia

Etiology: Old Age Macro: - Cortical atrophy - Enlarging ventricles (Compensatory hydrocephalus) - Thickening of Leptomeninges (Pia Mater & Arachnoid Mater) (The “Thin” Meninges) Clinical Features: - Dementia: All Spheres of Intellect affected

AGE-RELATED (SENILE) DEMENTIA

Most common cause of dementia Etiology: - Exact etiology Unknown - Genetic & Environmental Components - (Inevitable in Down-Syndromes) Pathogenesis: - Excess β-Amyloid Protein Formation (A Degradation product of Amyloid Precursors) Early Signs: (Neuronal Atrophy Starts in the Hippocampus) Memory Loss is : the First Sign Progressive Signs: (Neuronal Atrophy Progresses to the Cortex)

ALZHEIMERS DISEASE

β-Amyloid Protein Deposition around Neurons

Neuritic Plaques

β-Amyloid Protein Deposition in Blood Vessels

Amyloid Angiopathy

What clinical feature of Alzheimer's? § Increased Memory Loss § Confusion, Apathy, Anxiety § Difficulty Handling Money

Mild Cortical Atrophy

What clinical feature of Alzheimer's? § Difficulty Recognizing People § Difficulty with Language § Wandering & Disorientation

Moderate Cortical Atrophy

What clinical feature of Alzheimer's? § Seizures, Incontinence § Groaning/Moaning/Grunting

Late Signs: (Extreme Global Cortical Atrophy)

Treatment of Alzheimer's Disease? CLUE: AEI

Acetylcholine-Esterase Inhibitors

A clinical syndrome characterized by sudden onset of a focal neurological deficit presumed to be on a vascular basis; avoid ‘CVA’ (‘confused vascular assessment’)

STROKE

(80%) Results from focal ischemia leading to cerebral infarction. Mechanisms include embolism from heart or proximal arteries, small vessel thrombosis, or hemodynamic from a drop in the local perfusion pressure. Global ischemia (e.g. from cardiac arrest or hypotension) causes a diffuse encephalopathy.

Ischemic Stroke

(20%) Abrupt onset with focal neurological deficits, due to spontaneous (non-traumatic) bleeding into the brain. When blood vessels in the brain ruptures causing bleeding and damage to surrounding tissues.

Hemorrhagic Stroke

STROKE TERMINOLOGY: Amaurosis Fugax, Transient Monocular Blindness (TMB). Due to episodic retinal ischemia, usually associated with ipsilateral carotid artery stenosis or embolism of the retinal arteries resulting in a sudden, and frequently complete, transient loss of vision in one eye

Transient Ischemic Attack (TIA)

STROKE TERMINOLOGY: Stroke syndrome with a persisting neurological deficit suggesting cerebral infarction; the ensuing neurological defect can last days, weeks, or permanently; even after maximal recovery, at least minimal neurological difficulties often remain.

Completed Stroke (CS)

STROKE TERMINOLOGY: Neurological deficits begin in a focal or restricted distribution but over the ensuing hours spread gradually in a pattern reflecting involvement of more and more of the particular vascular territory.

Progressing Stroke (Stroke In Evolution)

inadequate perfusion of brain due to * an embolus from an atherosclerotic plaque in a large vessel (artery to artery embolus) (most common) * a large vessel thrombosis with low distal flow

Atherosclerotic Plaque