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Diseases of CNS: Brain
Trauma
Idiopathic vestibular disease
Neoplasia
Idiopathic epilepsy
Status epilepticus
Diseases of CNS: Spinal Cord
Intervertebral disc disease
Trauma
Atlantoaxial subluxation
Cervical spondylomyelopathy
Degenerative myelopathy
Discospondylitis
Ischemic myelopathy
Disease of PNS
Deafness
Metabolic neuropathy
Laryngeal paralysis
Megaesophagus
Tick paralysis
Facial nerve paralysis
Brain Trauma
Acute clinical onset from traumatic experience (HBC, Falling)
Injury to brain from:
Primary Event: Direct injury to nervous tissues
Secondary Event: Occur as result of primary trauma
Increased Cranial Pressure
Edema
Hypoxia
Seizures
Primary events may cause irreversible disruption of fiber tracts or reversible cell damage
Secondary events may cause herniation of Nervous Tissue through Foramen Magnum
What happens in the Primary Event of Brain Trauma
Direct injury to nervous tissues
What is the Secondary Event of Brain Tauma?
Occurs as a result of primary trauma
Secondary Event Brain Trauma happens because of
Increased intracranial pressure
Edema
Hypoxia
Seizures
Primary Events may cause
Irreversible disruption of fiber tracts or reversible cell damage
Secondary Events may cause
Herniation of nervous tissues through foramen magnum
CS of Brain Trauma
Hx of trauma to head
Seizures
Blood in ears, nose, oral cavity
Ocular hemorrhage
Loss of consciousness/ decrease in response to external stimuli
Signs of shock (Cardia Arrhythmias, Altered Resp. Patterns, Coma)
Dx of Brain Trauma
Hx & PE
Rads
CT or MRI
Tx of Brain Trauma
Aimed @ preventing/decreasing secondary effects of trauma
Correct any metabolic derangements
Provide oxygen
Elevate head
Admin osmotic agents to decrease cerebral edema:
Mannitol
Furosemide
Ain’t-seizure medication if needed
Corticosteroids for shock
Idiopathic Vestibular Disease
“Old Dog Vestibular Disease”
Abnormality of vestibular system due to unknown reason
Acute disorder of older aged (mean 12 years) dogs & cats
CS usually resolve in 3-6wks
CS of IVD
Loss of balance (incapacitating)
head tilt
Nystagmus
Disorientation
Ataxia
Circling/falling over
Anorexia
Dx of IVD
CS
Otic exam to rule out inner ear problem
BW to rule out other dz involving nervous system
Tx of IVD
Supportive Therapy
Anti-emetics
Motion sickness meds
IV fluids
Keep in confined padded area
Spontaneously resolves****
Head tilt may persist
Brain Neoplasia
Enlarging tumor in brain
Causes tissue compression &/ replaces healthy neuronal tissue
May be primary or metastatic
Most common in OLDER animals
CS progressive
Brian Neoplasia: Primary vs Metastatic
Primary: Typically Singular
Metastatic: May be singular or multiple
CS Brain Neoplasia
Reflect location
Progresses as tumor grows
Seizures
Endocrine derangements
+/- Vestibular signs
Tremors, Ataxia
Dx of Brian Trauma
Systemic screening for primary tumors in other organs
BW, Rads, Ultrasound
CSF tap
Increased pressure + albumin, Normal WBC count
Ophthalmic Exam:
Optic Nerve Edema
****CT or MRI****
Tx of Brain Neoplasia
Tumor
Sx removal
Radiation
Chemotherapy
CS:
Anti-seizure meds
Corticosteroids
Idiopathic Epilepsy
Repeated episodes of seizures with no cause
Seizures usually begins b/t 1-6 years
INCURABLE dz
CS of Idiopathic Epilepsy
Seizures, often at regular intervals
Young animals typically affected
Normal behavior b/t seizures
Dx of Idiopathic Epilepsy
1 of exclusion
BW to rule out Hypocalcemia, Hypoglycemia, Infection, Hepatic Encephalopathy, Lead Poisoning
Rads to rule out head trauma or hydrocephalus
CT or MRI to rule out space-occupying lesion
Tx of Idiopathic Epilespy
Initiated if seizure freq. more than once per month
Anti-seizure Meds:
Phenobarbital
Potassium Bromide
Zonisamide
Gabapentin
Keppra
Status Epilepticus
Continual seizures for prolonged period ( over 5-10 mins)
Medical EMERGENCY:
Can lead to irreversible coma and death!
CS of Status Epilepticus
Prolonged, uninterrupted seizure activity
Tx of Status Epilepticus
IMMEDIATE
Diazepam IV
Maintenance:
Anti-Seizure meds
Intervertebral Disc Disease
Disc protrusion/extrusion
Most common in cervical, caudal thoracic & lumbar spine
IDD Severity Depends On:
Speed @ which disc material is deposited into spinal canal
Degree & Duration: of compression
2 types of herniation
Type I: IDD
Acute rupture of annulus fibrosis & extrusion of nucleus pulposus in into spina canal
Common in YOUNGER dogs
Type II: IDD
Extrusion over longer period, prod. less acute & less severe CS
Common in OLDER (over 5 years) LARGE breed dogs
CS of IDD
Depends on location & type
Apparent pain
Presence/Absence of motor/sensory deficits
Paresis/Paralysis: May be unilateral or bilateral
Decreased panniculus reflex 1-2 vertebral spaces caudal to actual lesio
Altered deep pain response
Dx of IDD
Age, breed, CS, Hx
Compete Neurologic exam
Rads: Narrowed disc spaces @ location of lesion
Myelogram
MRI
Tx of IDD: Type I
Medical Tx:
Strict confinement for min. 2 wks
Corticosteroids
Intensive Nursing Care:
Soft padding in cage
Indwelling urinary catheter if necessary
Surgical Tx:
Fenestration, Hemilaminectomy
Reversed for animals w multiple episodes, ataxia, paresis/paralysis & absence of deep pain
Tx of IDD: Type II
Corticosteroids
Spinal Cord Trauma
Acute injury to spinal cord causing tissue injury
Direct & Indirect effects
Commonly resulting from: HBC, Gunshot wounds, Fights
Auto-dissolution of cord may be seen as early as 24hr after injure
Spinal Cord Trauma: Direct Effects
Due to primary disruption of neural pathways in cord
Spinal Cord Trauma: Indirect Effects
Triggered by direct effect
Edema, hemorrhage, ischemia, inflammation
Ischemia
Vesibular
CS of Spinal Cord Trauma
Hx of trauma
Presence of Schiff-Sherrington sign****
Lack of panniculus reflex causal to lesion
Paresis/Paralysis
Paresis
Paralysis
Schiff-Sherrington Sign
Rigid HYPERtonicity of front legs
HYPOtonicity of rear legs
Normal reflexes
Normal pain perception
Dx of Spinal Cord Trauma
Complete neuro exam to localize region
Rads
Myelogram
MRI
Myelogram
Tx of Spinal Cord Trauma
Medical:
Corticosteroids
Strict confinement for 6-8weeks
Surgical:
Initiate within 2hr if possible
Considered in severe paresis/paralysis cases or evidence of continuing cord compressing/worsening CS
Laminectomy @ all sites of cord compression
Removal of all bone frags/ disc material from spinal cord
Strict confinement: 2wks
Atlantoaxial Subluxation
Trauma when cranial portion of axis is displaced into spinal column
Displacement may be a result of:
Congenital/Development abnormalities
Trauma
Combo of both
Most common in YOUNG (Under 1 yr) TOY & MINI breeds of DOGS
CS of AAS
Reluctance to head pats
Neck pain
+ /- Tetra-paresis/ Tetraplegia
Sudden death! Due to respiratory paralysis
Tetra-paresis
Tetraplegia
Dx of AAS
Rads:
Lateral projection with neck in slight ventriflexion
Care must be taken to avoid further spina cord damage***
No anesthesia
TX of AAS
Medical:
Splint neck in EXTENSION
Strict cage confinement: 6 wks
Sx:
(IF neurological deficits/neck pain unresponsive to med tx)
Strabilization
Decompression
Combo of both
Cervical Spondylomyelopathy
Wobbler Syndrome
Cervical spinal cord compression as result of: CAUDAL VERTEBRAL (C5-C7) malformation/misarticulation
LARGE BREED DOGS:
Dobermans, Great Danes
Onset before 1 year in Danes, 2 years in Dobermans**
Progressive
CS of Cervical Spondylomyelopathy
Hx of progressive pelvic limb ataxia
Legs may cross, abduct widely, tend to collapse
Abnormal wearing of dorsal surface or back paws, nails, both
Swingling/wobbly gait in back legs (worse on rising)
Similar signs in front legs
+ /- Atrophy in front legs
Riding flexion of neck but NO NECK PAIN
Dx of Cervical Spondylomyelopathy
Rads, May Indicate:
Malalignment/ “Slipping” of vertebrae
Remodeling, new bone formation, narrowing of spinal canal
Myelography
Essential in locating regions of compression
CT & MRI
Tx of Cervical Spondylomyelopathy
Medical:
Anti-inflammatory doses of Corticosteroids
Neck brace
Cage confinement
Surgical:
Decompression:
Laminectomy/ Ventral Slot Procedures
Stabilization
Degenerative Myelopathy
Diffuse, irreversible degeneration of WHITE MATTER on ascending/descending tracts in ALL segments of spinal cord (Lesion most extensive in thoracic region)
Exact cause unknown (may be from autoimmune response to antigen in NS)
Seen mostly in GERMAN SHEPHERDS (over 5 years)
Progressive, INCURABLE dz
CS of Degenerative Myelopathy
Hx of progressive hind limb paresis & ataxia for 5-6 moths
Muscle atrophy
Dx of Degenerative Myelopathy
Neurological Exam:
Lesion in region *****T3-L3******
Decreased/Absent proprioception & placing reactions
Increased - Normal patellar reflexes
Lack of pain
Normal sphincter tone
Normal panniculus reflex
Rads:
May show dural ossification/narrowed disc spaces
CSF tap
May show increased protein concentration from lumbar subarachnoid space
Tx of Degenerative Myelopathy
NONE
Symptoms slowly progress until animal = nonambulatory
Discospondylitis
“Vertebral Osteomyelitis”
Bacteria/ Fungi implanted on bones of vertebral column
Implantation may occur:
**Most Common: Hematogenous Route
Penetrating wound
Paravertebral abscess/infection
Sx of vertebral column
Migration grass awns
CS Discospondylitis
Weight losss
Fever of unknown origin
Reluctance to excercise
Spinal pain
Hyperesthsia over lesion
+ /- Neurological signs
Dx of Discospondylitis
Rads:
May show destruction or lysis of bony end plates adjacent to lesion, osteophyte formation, collapse of intervertebral disc space
CBC: May show increased WBC count
Aerobic, Anaerobic, Fungal cultures of Blood, CSF, Urine
Sx biopsy & tissue culture
Tx of Discospondylitis
Long-term antibiotic/antifungal therapy ( at least 6wks, may be up to 6months
C&S
Pain Management
Sx?
Ischemic Myelopathy
Caused by fibrocartilagenous embolism
Necrosis of spinal cord gray & white fiber tracts when FCE obstruct veins & arteries in both leptomeninges & cord parenchyma
Reduced blood flow
Most common: LARGE & GIANT breed dogs
CS of Ischemic Myelopathy
Hx of mild-to-moderate exercise before development of CS
Acute onset of Neurologic signs:
May appear progressive @ first, but stabilize after first 24 hrs
Lack of acute spinal pain associated with Neurologic sign
Paresis or spastic paralysis of limb
Reluctance to move, inability to rise
Dx of Ischemic Myelopathy
Based on excursion:
Rads, CBC, CSF usually WNL
MRI
Tx of Ischemic Myelopathy
Corticosteroids
Nursing Care: May take months to recover
Peripheral Neuropathies
Represented clinically by a group of signs
Neuropathic Syndrome
Signs Include:
Reduced/ Absent muscle tine
Weakness (paresis) / paralysis of limb / facial muscles
Followed by neurogenic muscle atrophy in 1-2 wks
May involve a single nerve or multiple
Deafness
Inability to hear
May be central or peripheral origin
Conductive deafness
Hereditary or congenital, related to drug therapy, or normal aging
Permanent / Irreverible
Deafness: Central Origin
From damage to CNS & auditory pathways
Deafness: Peripheral Origin
From cochlear abnormalities
Conductive Deafness
From chronic otitis, rupture of tympanic membrane, damage to middle ear
This medicine can cause deafness
Mometamax
CS of Deafness
Lack of response to auditory stimuli
Excessive sleeping
Prone to deafness
Bull terriers, Dobermans, Dalmatians, Rotts, Pointers, Aussies, BLUE EYED WHITE CATS
Dx of Deafness
Partial loss hearing & unilateral complete loss of hearing difficult to est. clinical exam
Inability to abuse sleeping pt with loud noise
Behavior evaluation
Stimulate with various sounds from diff. Directions
PE of external ear canal & tympanic membrane
Deafness: Electrodiagnosis
At specialty clinic
Tympanometry
Acoustic reflex testing
Auditory evoked responses (BAER)
Tx of Deafness
None
Hearing aids?
Laryngeal Paralysis
may be hereditary, acquired, idiopathic
*****Care must be taken when examining animal w suspected laryngeal paralysis
Hereditary: Laryngeal Paralysis
Bouvier does Flanders & Siberian Huskies
Acquired: Laryngeal Paralysis
From lead poisons, *RABIES, trauma, inflammatory infiltrates of vagus nerve
Idiopathic: Laryngeal Paralysis
In MIDDLE-TO-OLD aged LARGE to GIANT breed dogs
CS of Laryngeal Paralysis
Inspiratory stridor
Respiratory distress
Loss of endurance
Voice change
Cyanosis
Complete respiratory collapse
Stridor
Dx of Laryngeal Exam
Laryngeal Exam
Laryngoscopy: shows Laryngeal Abductor Dysfunction
Tx of Laryngeal Paralysis
Sx
Arytenoidectomy
Arytenoid lateralization
Removal of vocal chords
Megaesophagus
Lack of effective esophageal peristalsis, resulting in dilation of esophagus, regurgitation of undigested food
Congenital, Hereditary, Acquired
Congenital: Megaesophagus
Great Danes, German Sheps, Irish Setters, Newfoundlands, Sharpeis, Greyhounds
Usually becomes evident around WEANING
Hereditary: Megaesophagus
Wire-haired fox terriers & mini schnauzers
Acquired: Megaesophagus
May be due to metabolic neuromuscular dz, distemper, tick paralysis, lead poisoning, laryngeal paralysis -polyneuropathy complex, or polymyositis
CS of Megaesophagus
Regurgitation of undigested food
Respiratory Signs:
Cough, Dyspnea, Drooling, Pneumonia
Lack of growth / Weight loss
Dx of Megaesophagus
Rads: Dilated esophagus to level of diaphragm
Tx of Megaesophagus
NO CURE: Prevent development of aspiration pneumonia
Elevated feeding platform
Liquid soft diet high in caloric density
Several small feedings daily
Treat any underlying metabolic disorders
Tick Paralysis
Flaccid, Afebrile, Ascending motor paralysis
Caused by common dog tick (Dermacentor Variablis) & Rocky Mt. Wood Tick (Dermacentor Andersoni)
Female tick = salivary neurotoxin that interferes w acetylcholine concentrations @ neuromuscular junction
Cats RESISTANT
CS of Tick Paralysis
Gradual development of hind limb in coordination → flaccid ascending paralysis
Within 24-72hr, may become recumbent
Reflexes lost while sensation remains
Death may occur due to respiratory paralysis
Presence of ticks on dog
Dx of Tick Paralysis
Based on exclusion
Based on response to tick removal
Tx of Tick Paralysis
Remove all ticks
Supportive care
Facial Nerve Paralysis
Idiopathic, acute paralysis of facial nerve
Seen in adult dogs & cats (Over 5 years)
Cause unknown