Encephalopathy Flashcards
Clinical presentation metabolic encephalopathy
Signs are symmetric and diffuses, can wax and wane and progress based on he underlying condition
Hepatic encephalopathy
Underlying liver disease : liver failure or shunt
Pathophysiology : ammonia, short fatty acid or other gut-derivated toxin and cause neurotoxicity. Can alter amino-acid metabolism and induce formation of false neurotransmitters or cause production of false neurotransmitters. Reduced serotoninergic neurotransmission. Imbalance between GABA (inhibitory neurotransmitter) and glutamine (excitatory neurotransmitters).
Clinical signs: obtunded mentation, abnormal behavior, compulsive pacing, head pressing, visual deficits and seizure. Cats with PSS are more likely to have seizure vs dogs and often exhibit ptyalism as a characteristic clinical signs. Other signs are related to liver failure. Clinical signs might wax and wane in association with eating (moreso high protein meals)
Treatment: see GI notes
Renal associated encephalopathy.
Include uremic encephalopathy, dialysis disequilibrium syndrome and post transplantation encephalopathy
The cause of uremic encephalopathy is unknown but suspected mechanisms includes increased circulating neurotoxins, increased PTH levels, hyperosmolality and hypertension.
Clinical signs include abnormal mentation (ranging from obtundation to coma), seizure activity. Other signs includes muscle tremor, generalized weakness and irregular respiration.
Treatment : management of the underlying renal disease (electrolyte imbalance and acid-base imbalance) and hypertension.
Hypoglycemic encephalopathy
Possibles causes of hypoglycemia
- Toy bread hypoglycemia (glycogen depletion in neonatal/juvenile)
- Hunting dog hypoglycemia syndrome
- Glycogen storage disease.
- Insulinoma
- Sepsis
- Liver failure
- Hypoadrenocorticism.
- Insulin overdose
Electrolyte associated encephalopathy
Imbalance of calcium or sodium
Sodium :
— Hypernatremia : causes the brain cells to shrink due to osmotic pull. Over time (>48-72 hours) idiogenic osmoles will be created in the brain cells to equilibrate osmolality.
—Hyponatremia : results in cerebral oedema.
Treatment : do not correct at a higher rate than 0.5 mEq/L/hr.
— With hypernatremia, the risk is to cause cerebral oedema due to osmotic pull from idiogenic osmoles.
— With hyponatremia, risk is a loan shrinkage and demyelination, predominantly in the thalamus —> myelinolysis. This syndrome is delayed by several days to 1-2 weeks.
Calcium
— Hypercalcemia : can cause decreased excitability of the neuronal cells and direct toxic damage.
— Hypocalcemia : can cause increased excitability of the cell membranes and problem with neurotranmission.
Treatment
— hypo : calcium gluconate acutely, long term calcium and vitamin D supplementation.
— hypercalcemia: diuretics (normal saline) and furosemide.
Thiamine deficiency encephalopathy
Cause : thiamine deficiency will lead to insufficient ATP production —> neuronal dysfunction and death if not treated.
Usually enough thiamine in diet but fish contains high levels of thaminase
Onset is acute and rapidly progressive.
Clinical signs include vestibular ataxia, decreased mentation, ventroflexion, seizure activity, pupil dilation, absent menace response and head tremor. Can lead to coma and opisthotonus.
Necropsy : characteristic bilateral symmetric lesions (petechial hemorrhage)
Bacterial meningoencephalitis
Pathophysiology : bacterial infection can produce mass effects secondary to abscess formation vs release of bacterial endotoxins. The main neurological deficits are secondary to inflammatory response induced by the bacteria.
Most common implicated organisms : staphylococcus, streptococcus, pasteurella, actinomyces, nocardia, e.coli, klebsiella and anaerobic.
Clinical signs : often acute and rapidly progressive. Fever and cervical hyperesthesia are considered classic.
CSF analysis : suppurative with degenerate and toxic neutrophil.
Treatment
— IV antibiotic : Ampicillin (broad spectrum, bactericidal), enrofloxacin (for gram negative agents), cephalosporin third generation (gram positive agents) or metronidazole (anaerobic)
— Oral antibiotics : TMS (broad spectrum and bactericidal) vs oral version of atb just listed.
Fungal meningoencephalitis
Most common agents : cryptococcus, coccidioides, blastomycosis, histoplasmosis, aspergillus, crytococcus neoformans. Crypto is by far the most common in cats and dogs.
Clinical signs are secondary to mass effect (granuloma) vs secondary to the inflammatory response
Presentation: can be acute onset but often is characterized by a slow progression (week to months) of neurological dysfunction, often preceded by a period of non specific illness. Clinical evidence of extra neural fungal infection is common.
Treatment : few antifungal drugs are able to cross the BBB even when inflamed. Flucytosine (5-fluorocytine) and fluconazole (thiazole) are two antifungals that readily cross the BBB. Risk of drug resistance with flucitosine used alone. Itraconazole DOES NOT cross the BBB.
Viral meningoencephalitis
Most common one are canine distemper (paramycovirus) and FIP (coronavirus)
Other less common : FIV (lentivirus), rabies, canine herpesvirus, panleukopenia virus.
Clinical signs might be acute to subacute but might be peracute (pseudorabies) or insidious (FIP)
Multifocal encephalopathy are common but evidence of focal brain dysfunction may also occur. Extraneural signs (eg. fever, ophthalmic disease, respiratory disease) of viral infection can be present.
Protozoal encephalopathy
Dogs : Toxoplasma gondii and Neospora caninum.
Cats : Toxoplasma gondii.
Neurological dysfunction is thought to be caused by the intracellular proliferation of tachyzoites.
The onset of clinical signs can be acute or chronic. Deficits can be multifocal or focal
Rickettsial meningoencephalitis.
Only in dogs ; GS seems to be predisposed
Secondary to Ehlichia canis or Rickettsia rickettsii (RMSF)
Clinical manifestation : focal and multifocal signs of encephalopathy. Central vestibular disease is a common presentation. Clinical signs of systemic illness are common.
Recommendation for treatment is doxycycline.
Intracranial neoplasia
Clinical signs are acute (associated bleeding ; threshold size) or gradual (due to slow growth) in onset.
Primary brain tumor
— Meningioma : most common brain tumor in cat, in dogs dolicephalic dogs are overrepresented.
— Glioma : brachycephalic dogs are overrepresented.
— Pituitary adenoma/adenocarcinoma
Prognosis for glioma are more guarded.
Secondary brain tumor
— tumor of the skull - multilobular osteochondrosarcoma, chondrosarcoma, osteosarcoma.
— Extension of nasal/frontal tumor
— Lymphosarcoma
— Metastatic carcinoma —> mammary, prostatic and pulmonary
— Hemangiosarcoma
— Malignant melanoma
Feline ischemic encephalopathy.
Cause : intracranial cuterebra migration.
Clinical signs : history of respiratory disease is common, likely due to migration of the larva through the nasal cavity and cribiform plate. Focal or multifocal intracranial signs, typically asymmetric. Usually combination of seizure, circling, altered mentation, menace/response deficits. Onset is acute/peracute, usually non progressive.
Treatment : ivermectin is controversial
Intracranial hemorrhage/infarction
Causes :
— hypertension
— TE disease
— arthrosclerosis
— septic or neoplastic embolism
— aberant parasite migration
— coagulation disorders
— Neoplasia
— Trauma
Recovery : cases that show potential for recovery usually show some amount of visible recovery within the first 2 weeks post-event.
Granulomatous meningo-encephalitis
Common inflammatory disease in dogs - very rare in cats.
Suspected to be auto-immune T cell mediated hypersensitivity reaction.
Lesions predominated in the white matter.
Young to middle aged female dogs or small breed dog apprear to be predisposed.
Clinical presentation
— Multifocal : acute onset, rapid progression.
— Focal : more incidious, rapid progression.
Clinical signs includes seizures, cerebrovestibular dysfunction or cervical spinal hyperesthesia. Other forebrain signs are relatively common as well.
Treatment
— Lifelong immunosuppressive therapy
— Steroids
— Other drugs : Cytosar, CCNU and cyclosporine
Prognosis
— Longer for focal lesions than multifocal and diffuses.
