Bilateral inflammation of motor branches of CN-V

demylinantion

acute onset inability to close the jaw

facial sensation generally normal

Improvement will be seen within 2-3 weeks

If no improvement seen, may have missed lymphoma

inflammatory muscles of mastication

Pain in muscles

Difficulty opening the mouth

Unilateral

droppy face, no palpebral reflex, manace reflex only with 3rd eyelid 

Blood filled space on either side of pituitary gland

Motor innervation to extraocular muscles

no manance

PLR present

Ventral nerve roots develop most severe pathology

Dorsal nerve roots essentially spared

=

Severe paresis or plegia with preservation of pain sensation; hyperesthesia

Initial stiff, stilted short strided gait

LMN tetraparesis/plegia, dysphonia

NO smooth muscle/autonomic involvement; CN normal

Fecal and urinary incontinence uncommon

No megaesophagus

Tx: intensive physical therapy

NO STEROIDS

Rapid onset

LMN paresis starting in pelvic limbs → recumbant in 24-72 hours

No cranial nerve involvement or megaesophagus

Response to Frontline

Recovers 24-72 hrs 

Do NOT use doxycyline

Muscular weakness and fatigability

Auto-antibody mediated destruction of Ach receptors at the NMJ

After activity-paresis in pelvic limbs

Regurgiation, drooling, eyelid and lip paresis

Megaesophagus

Spinal reflexes are generally normal

Suddent onset of megaesophagus and severe regurgitation

Rapidly progressive tetraparesis, loss of spinal reflexes

Tensilon response test

AchR autoantibody test

Tx: Anticholinesterase agents - Pyridostigmine, neostigmine

Immunosuppressive medications: corticosteroids, mycophenolate, cyclosporine, azathioprine

Broad spectrum antibiotics for aspiration pneumonia

Proton pump inhibitors for esophagitis

Young/middle aged purebreed dogs

Acute

3 forms: focal, disseminated, ocular

Most common form

acute

white matter predilection: cerebral, cerebellum, caudal brain stem, cervical cord

Multifocal, necrotizing, nonsuppurative encephalitis

Yorkies- 4.5 years

Lesions in cerebrum and brainstem

Chronic, progressive, relapsing, remitting

Deep white matter of the cerebrum, thalamus, and brainstem

Cavitation, necrotic axons, gliosis, gitter cells

Usually subacute/chronic. 

Peripheral vestibular dz

Dogs > 8 years, cats (bilateral) of any age

acute/peracute onset of unilateral nonprogressive peripheral vestibular signs

No Horner's/facial n. deficits present

Tx: anti-emetics, seadtives, IV fluid support

Steroids do NOT improve recovery

Cats >> dogs

No head tilts, no nystagmus, lack of normal physiologic nystagmus

Crouching posture, reluctance to walk

Chronic, progressive history (can be acute)

Often other cranial nerve signals

central vestibular disease

Antagonism of GABA in the CNS (Valium - speeds recovery)

Acute onset central vestibular sight +/- seizures (more common in cats) and other forebrain signs

occlusions of vessel

Thrombus/thromboembolism

Deprives tissue of oxygen and glucose

50% may be related to unrelated medical condition

Rupture of vessel → bleeding into surrounding brain tissue → hematoma → compression of adjacent tissues leads to clinical signs (brainstem = vestibular signs)

rare in dogs

acute onset, nonprogressive clinical signs

geriatric patients

clinical signs usually begin to improve in 24-72 hours

Perinatal infection causes destruction of external germinal layer prevents formation of granular layer

Nonprogressive

Congenital malformation 

Absence/hypoplasia of cerebellar vermis → concurrent hydrocephalus

cerebellar ataxia, tremors, absent menace at 3-4 months of age

nonprogressive

Affects younger animals

Cause compression of 4th ventricle and obstructive hydrocephalus

Caudal occipital malformation syndrome

Congenital hypoplasia of the supraocipital bone→caudal fossa small compared to entire cranial cavity→cerebellar identation and heirniation→kinking of medulla→loss of dorsal subarachnoid space at the craniocervical jxn→dural/fibrous band and the craniocervical jxn→alterations in CSF flow out the foramen magnum

Toy breed and brachycephalics predisposed

Clinical signs 3-12 mo of age

severe cases may be incidental finding 

sunset strabismus, seizures, abnormal behavior, mentation change

Often symmetrical: circling, central blindness, postural reactions deficits 

Tx: diuretics, mannitol in emergencies, proton pump inhibitors, corticosteroids

Insert a shunt surgically

Toy breed dogs

may progressively enlarge (signs develop in older animals) or be static - usually incidental

Generalized seizures-occipital cortex

sepsis, liver failure, insulin overdose, xylitol toxicity

weakness/lethargy and seizures

<3 years old at diagnosis

low albumin, glucose, cholesterol and BUN

microcytic anemia; bile acids >100 post prandial

Elimination of gut derived toxins

Lactulose: lowers colon pH to prevent ammonia absorption

Antibiotics to redcuce colonic bacterial flora