Intoxications and Infections of the Nervous System Flashcards
Tetanus (demented monkeys)
- prevent release of inhibitory GABA
- prolonged painful muscle spasms
- localized vs generalized (diffuse mu spasms and generalized convulsive seizures from cortical disinhibition)
painful muscle spasms of tetanus
- clenching lockjaw (trismus)
- grimacing smile (risus sardonicus)
- arching back (opisthotonus)
Botulism (robots)
- improperly canned or contaminated food or in wound infections
- prevent release of ACh from LMN and parasympathetic nerves=paralysis of skeletal muscle, bowel, bladder, and salivary glands
Guanidine
oral drug helps facilitate ACh release from motor nerve endings
Environmental toxins
- lead poisoning: adults-peripheral neuropathy + focal neuropathy (wrist drop); kids-encephalopathy and abdo pain
- organic solvent/glues and adhesives: peripheral neuropathy +/or encephalopathy
- CO-HA, v, blurry vision…coma, sz, cardiopulm arrest. survivors: memory and cognition deficits, parkinsonism
what should a stroke syndrome in a young, otherwise healthy, pt make you think of?
drug induced vasoconstriction or HTN leading to ischemic infarction or brain hemorrhage. **cocaine
Alcohol withdrawal
- hypersympathetic stage-tremulousness, sweating, tachy, jitters
- 12hr-3d after last drink: cluster of generalized tonic-clonic seizures (d/t diffuse toxic effect on the brain)
- 3-4d after last drink: DTs
what provides sedation and seizure control for DTs
benzos
Wernicke-Korsakoff syndrome
- B1 (thiamine) deficiency in pts with malnutrition or malabsorption
- acute phase: W’s encephalopathy=nystagmus, ophthalmoplegia, gait ataxia, and confusion (resolve in hours to days of thiamine administration)
Korsakoff’s psychosis
- 2/2 persistent, severe, or recurrent thiamine deficiency
- chronic memory deficit or amnestic syndrome leading to confabulation
pathology of Korsakoff
-tiny petechial hemorrhages and gliosis around 3rd and 4th ventricles and connecting aqueduct, involving mammilary bodies, fornix, and dorsomedial thalamus
alcoholic cerebellar degeneration
-involves anterior-superior vermis=ataxic gait and dysmetria of the lower limbs
central pontine myelinolysis
- 2/2 overly rapid correction of severe hyponatremia
- get demyelination of the corticospinal and corticobulbar tracts in the pons
where can meningitis come from
-can directly spread form an infection in an area near (ex otitis or sinusitis) or f/m infectious organisms spread through the bloodstream from a remote infection (PNA)
acute meningitis
- fever, HA, stiff neck, malaise, lethargy, n/v
- acute bacterial meningitis can be fatal!!
what causes neck stiffness/nuchal rigidity?
- meningeal irritation or inflammation
- can cause signs of Kernig or Brudsinski
what is initial Abx coverage for meningitis
ceftriaxone and vancomycin (add Ampicillin to cover for Listeria)
role of iv dexamethasone (0.15mg/kg)
- reduces neuro complications
- lowers mortality
- give just before/with initial abx
When substantial amt of purulent exudate or pus develops from bacterial meningitis what can it cause
hydrocephalus by obstructing CSF pathways
meningoencephalitis
when pus accumulates over the cortical subarachnoid space and leads to inflammation and edema of the cortex itself…can also get infraction of underlying brain or SC when local superficial blood vessels become inflamed and thrombose
what should young kids recovering from meningitis be observed for
subsequent deafness which may impede their ability to learn to talk
LP
-perform asap in meningitis management
reasons to delay an LP
- thrombocytopenia
- deficient clotting factors
- infection along skin of the back
- elevated ICP
- intracranial mass with edema (new onset sz, focal neuro deficit, h/o stroke, IC)
what is the most typical profile for bacterial meningitis
PMN WBCs and low CSF glucose
encephalitis primary site of infection and indllmation
THE BRAIN
modes of infection by the causative virus of the encephalitis
- arthropods (ticks, mosquitoes)
- ingestion (polio virus)
- inoculation (Rabies from animal bites)
- inhalation
- reactivation (Herpes simplex)
encephalitis microscopically
neuronal destruction by proliferating microglia, perivascular lymphocytes, and viral inclusions within neurons and glia
are antiviral drugs useful in encephalitis
only herpes simpex wherein acyclovir is used
HSE
- 2/2 HSV1
- involves inferior frontal and medial temporal lobes, often b/l an asymmetric
whatre s/s highly suggestive of HSE
- aphasia
- behavioral changes
- memory deficits
polio
- viral invasion and destruction of anterior horn cells and BS motor nuclei
- asymmetrical LMN signs
- postpolio muscular atrophy in contra stronger limb
Zoster or shingles
- eruption of a vesicular rash with severe neuralgic pain along 1 or 2 adjacent dermatomes on torso or limb
- admin acyclovir
- sequelae: post-herpetic neuralgia
HIV1
destroys T4 helper lymphocytes
later sequelae of AIDS
-chronic painful sensory neuropathy along with cognitive changes, HIV dementia and myelopathy
AIDS and primary cerebral lymphoma
-PCL is a rare immune system tumor arising within the brain and most often occurs in AIDS pts
common opportunistic infections in AIDS
- cerebral toxo (protozoal parasite)
- cryptococcal meningitis (fungal)
- CMV retinitis or encephalitis
PML
- progressive multifocal leukoencephalopathy
- most cases occur in AIDS pts
- involves reactivation of latent JC virus (polyomavirus)–goes on to infect oligodendrocytes=patchy demyelination of CNS white matter=focal neuro deficits
What is an abscess?
- a localized encapsulated infection within or outside (epidural or subdural) the brain or spinal cord
- usually bacterial, but may be fungal or parasitic in IC pts
- may be solitary or numerous
How does an abscess develop
-f/m adjacent infection
OR
-through bloodstream from a distant infection
cerebral abscess may cause…
- seizures and focal neurological signs dependent on its location
- may create brain edema with mass effect and increased ICP
- may rupture into ventricular system or subarachnoid space and produce meningitis
how is the diagnosis of abscess confirmed
-CT or MRI brain scan with and without contrast
Prion dz
-prions=infectious proteins that can cause transmissible spongiform encephalopathies in human and animals
Creutzfeldt-Jakob dementia
- most common prion dz, sporadic
- v. rapidly progressive dementia with cerebellar, corticospinal, LMN or EPS s/s
- myoclonus is usually present
EEG of CJD
periodic sharp wave discharges
diagnostic brain bx of CJD
- spongiform changes which are cytoplasmic vacuoles in neurons and astrocytes
- neuronal loss sans inflammation
mad cow dz
bovine spongiform encephalopathy thats an epidemic prion dz in cattle
HSV encephalitis
- affects mostly temporal lobe and may present acutely (<1wk duration) with focal neurological findings
- csf: lymphocytic pleocytosis, inc erythrocytes, elevated protein
- standard for diagnosis: HSV PCR analysis
Creutzfeldt-Jakob dz probably diagnosis
- rapidly progressive dementia
- two out of 4:
- –myoclonus
- –akinetic mutism
- –cerebellar or visual disturbances
- –pyramidal/extrapyramidal dysfunction (hypokinesia)
- periodic sharp wave complexes on EEG and.or positive 14-3-3 CSF assay
CJD definitive diagnosis (need 2/4 features) and
-brain biopsy (gold standard) or demonstrated PRNP gene mutations
autonomic dysfunction
- postural hypotension
- abnormal sweating
- disturbance of bowel or bladder control
- abnormal salivation or lacrimation
- impotence
- gastroparesis
