Encephalopathies Flashcards
what is the ascending reticular activating system in the brainstem? purpose?
- what is mental status governed by, and when can it get messed up?
- ARAS channels sensory input from body to activate cortex
- Measures response to environment
- Mentation: awareness vs arousal
<><> - Mental status is a function of two major areas in the brain: the brainstem and thalamo-cortex
- Normal mentation: any time sensory input comes in, it is transmitted through ARAS (reticular formation, in the brainstem) and then the response to environmental stimuli is coordinated
o Abnormal mentation results with an abnormality in the brainstem or thalamo-cortex
Mentation: Responsiveness
- what are awareness vs arousal
awareness:
- bright, alert, responsive
- disoriented / dissociated
- demented / delirious
<><><><>
Arousal:
- BAR
- depressed / obtunded
- stuporous
- comatose
Depressed/obtunded vs stuporous vs comatose?
- signs, and parts of the brain that are affected?
Depressed/obtunded:
- Drowsiness, inattention, less responsive to environment
- Brainstem (ARAS), Thalamocortex
<><><><>
Stuporous:
- Unconsciousness + decreased responsiveness - Can be aroused with noxious stimulus
- Partial disconnection
- Brainstem (ARAS)
<><><><>
Comatose:
- Unconsciousness + NO responsiveness
- Total disconnection
- Reflexes may be intact
- Brainstem (ARAS)
disorientation can be due to abnormalities in what structures?
Thalamocortex &/or vestibulocerebellar
thalamus vs cortex lesions - how to distinguish on neuro exam
- we cannot!
Thalamocortex: NE, what we see if lesion
- Mentation: depression / delirium / disorientation / Δ behaviour
> Head pressing, compulsion, wandering, pacing
<><><><> - Gait & Posture: circling (ipsi), body turn (ipsi torticollis or pleurothotonus)
> Mild hemiparesis (contra)
<><><><> - Cranial Nerves: menace & nasal septum response deficits (contra)
<><><><> - Postural Reactions: Contralateral proprioceptive deficits with near-normal gait
<><><><> - Spinal reflexes: Normal
<><><><> - Palpation (Spinal Pain): possible neck pain
<><><><> - Seizures are always a sign of thalmo-cortex disease
Clinical Signs of Brain Dysfunction – Brain Stem
- Mentation: Depressed/stupor/coma
<><> - Gait and posture:
> Tetraparesis/plegia vs hemiparesis/plegia (UMN signs)
> decerebrate rigidity (hyperextension of front limbs and head, poor prognosis) and/or opistothonus
> vestibular ataxia (central)
<><> - Cranial nerves:
> Deficits in cranial nerves III-XII
<><> - Postural reactions:
> All four limbs ipsilateral deficits
<><> - Spinal reflexes: Normal
<><> - Palpation: Neck pain on palpation is possible
Encephalopathy: Clinical Signs
- what anatomy may be affected?
- lesion localization?
- Thalamocortex ± Brainstem ± Cerebellum
- Lesion localization: diffuse vs multifocal
<><><><>
Beware the focal lesion: - Extensive mass invading multiple CNS regions
- Focal lesion w/ extensive 2nd surrounding edema
- Focal obstruction of CSF flow > hydrocephalus
Encephalitis - what is it? categories?
- Result of inflammatory/infectious conditions, which in the CNS commonly affect several areas
> Encephalitis: brain
> Myelitis: spinal cord
> Meningitis: meninges
> Various combinations possible, e.g. meningoencephalitis, meningomyelitis,etc. - Both infectious and non-infectious causes
issues with what structure are responsible for pain in encephalitis cases?
meninges is the painful part, spinal cord and brain have no pain receptors
Infectious Encephalitis - common causes
- Viral: canine distemper, FIP (cats), rabies
- Rickettsial: Ehrlichia canis, RMS
- Bacterial: Staph, Strep, coliforms
- Fungal: blasto, histo, crypto, coccidioides, aspergillosis
- Protozoal: Toxoplasma, Neospora
- Parasitic: verminous, larval migrans, cysticercosis…
Non-infectious Encephalitis
- etiology
- prevalence in dogs vs infectious
- types, what we can call it with vs without histopath dx
- tx
- Immune-mediated
- Dogs (Canada): more common than infectious
<><><>
Without histopath: - Meningoencephalitis of unknown etiology (MUE)
<><>
With histopath: - Granulomatous meningoencephalomyelitis (GME) vs Necrotizing encephalitis (NE)
<><>
Treatment: - Immunosuppression > Steroids ± others
Granulomatous meningoencephalomyelitis (GME)
- what anatomy is affected? distribution?
- what animals are affected?
- prognosis?
- Brain, spinal cord, meninges
- Focal vs multifocal vs ocular (CN II)
- Mostly dogs (cats tend not to have this issue) > Any age, breed: tendency to small & 3-5y
- Prognosis: guarded to poor
Necrotizing Encephalitis
- who gets this?
- signs?
- prognosis?
<><>
- categories based on affected anatomy, and who is affected?
- Small breeds, younger age (2-5y)
- Seizures
- Prognosis: poor to grave
<><><><> - Necrotizing Meningoencephalitis (NME)
> Cerebral grey + white matter, meninges
> Pug, Maltese, Chihuahua, etc.
“pugs are the ememy (NME)”
<><> - Necrotizing Leukoencephalitis (NLE)
> Brainstem, cerebral white matter
> Yorkshire Terrier & French Bulldog
Encephalitis: Diagnostic Tests
- CBC / chem / UA, Thoracic rads, abdominal ultrasound
> Non-infectious: NAF
<><><><> - MRI: best, very sensitive to soft tissue changes, can see any inflammation/edema due to encephalitis
- CSF analysis: increased inflammatory cell count and protein levels, but non-specific
- Titres, PCRs based on suspected infectious disease
- Histopathology gives a definitive diagnosis
