NEUROLOGY WEEK 1 Flashcards
A head tilt is often due to
Vestibular disease
A head turn is often due to
Forebrain disease (turned towards sign of lesion)
Decerebrate body posture is ___.
Is indicitive of a lesion where?
Extention of all limbs and opistontonosis (exten of head/neck). Associated with stuperous./ comatose state.
Decerebellate body posture is ____.
Is indicitive of a lesion where?
DecereBELLATE is opthistonosus with thoracic limbs extended but hips flexed. Mentation normal. Indicitive of Cerebellar lesion
Schiff-Sherrington posture is ___.
Indicitive of a lesion where?
Acute severe thoracic/ cranial lumber spinal cord lesion. \
Extensor of thoracic limbs
Paralysis of Pelvic limbs (reflex preserved)
UMN Paresis gait
Muscle tone and Spinal reflexes - Normal to increased tone caudal to lesion
LMN Paresis gait
Muscle tone decreased. Bunny hopping / Knuckling.
The spinal cord is split into what 4 sections for localisation of lesions
C1-C5
C6-T2
T3-L3
L4-Cd
Which nerve does the Biceps tendon reflex test
Musculocutaneous (C6-C8)
Which nerve does the Triceps tendon reflex test
Radial n (C7-T2)
Which nerve does the Patellar tendon reflex test
Femoral n (L4-L6)
Which nerve does the Gastroc tendon reflex test
Sciatic n (L6-S2)
The pelvic limb withdrawal reflex tests which nerve and spinal cord segment
Sciatic nerve. L6-S2. (same as Gastroc tendon reflex)
Pathway for the Menace response
Is a CORTICAL response.
II–>Forebrain–>Cerebellum–> Brainstem–> VII
Pathway for the PLR reflex
Is a SUBCORTICAL response.
II–>Brainstem–>III
Pathway for Palpebral reflex
Facial sensation.
V –> Brainstem –> VII
Inability to close the jaw would be indicitive of a lesion in which CN
Trigeminal control motor to muscles of mastication.
Atrophy/ Inability to close the jaw.
Difference between a Simple focal and Complex focal seizure
Simple focal: no loss of consciousness
Complex focal: impairement of consciousness
Status Epilepticus is a seizure for > ___min
Seizure lasting more than 5 minutes (clinical)
More than 30 minutes = brain damage
Define cluster seizure
> 2 seizures in 24 hour period = serious.
Define Prodrome, Aura, Ictus and Post-ictal
Prodrome: Behaviour changes that happen days/hours before seizure
Aura: Sensory/Focal onset on seizure (difficult to see in animals)
Ictus: Seizure event
Post-Ictal: Neurological alterations post seizure
5 finger neurology rule
- Onset
- Clinical curse
- Pain
- Lateralising
- Neurological localisation
Which DAMINNT cause Lateralisation?
Degenerative, Neoplastic, Inflamm/Infectous, Trauma/ Vascular
What does DAMNITV stand for
Degenerative, Anomaly, Metabolic, Neoplastic/Nutritional/ Inflamm/Infectious/Idiopathic/Trauma/Toxic/ Vascular
Which DAMNITV cause pain?
Degenerative, Neoplasia, Infect, Inflamm, Trauma , Vascular
Which DAMNITV cause acute onset
Trauma, Toxic, Vascular
Waxing and Waning onset is especially indicitive of which type type of neuropathology
DAMNITV. Metabolic causes waxing and waning onset. Also not painful and not lateralising.
Acute onset but improving rather than deteriorating is indicitive of what…
DAMNITV. Trauma/Vascular tend to improve over type post acute onset. Also painful.
If Menace response is abnormal but palpebral reflex normal, what does this tell you about CN VII
Menace: CN II -> Forebrain –> Cerebellum–> Brainstem –> CN VII
Palpebreal: CN V–> Brainstem –> CN VII
Tells you facial nerve is normal.
Which crystals in urine are highly suggestive of a portosystemic shunt
AGE= METABOLIC = WAXING AND WANING
Ammonium biurate crystals (sharp crystals_ = highly suggestive
Also biochem = low liver enzymes/ creatinine/cholesterol. Related to feeding?
Diagnostic tests for portosystemic shunt
Ultrasound liver/ biochem/ Fasting bile acids
In human epilepsy patients, over expression of ___ is thought to change local brain uptake
Over expression of p-glycoprotein (PGP)
= PharmacoRESISTANT epilepsy in humans
When to start epilepsy treatment
More than 1 seizure every 6 weeks. Or more isolated within 6 weeks.
Status epilepticus or cluster seizures (within 24 hr period)
CHRONIC DISEASE
Treatment of Status epilepticus
Status: Seizure >30 mins in duration (or >5 mins clinicalls)
Benzodiapines or Phenobarbitone
How do Barbiturates/ Benzodiapines work for treatment of status epilepticus?
Barbiturate: Increase durating of Cl- channel opening. increased EFFICIENCY
Benzodiaz: Increased frequency of Cl- = Increased POTENCY
What effects would you expect to see on biochemistry on phenobarbital epilepsy treatment?
ALP elevation is common.
Side effects: Sedation, PD, Polyphag, Hepatotoxicity (metabolised by liver).
ROUTINE BIOCHEM BILE ACID STIM q 6 mnts
What tests should be done every 6-12 months on phenobarbital treatment
MONITOR phenobarb levels.
Routine biochem (raised ALP is common)
Bile acid stim test
Which rare but severe idiosyncratic reactions can occur with phenobarbital treatment.
What action should be taken?
Behavioural alterations.
Immune mediated neutropenia, thrombocytopenia, anaemia secondary to bone marrow necrosis.
Superficial necrolytic dermatitis.
STOP DRUG IMMEDIATELY
How does the time to steady state vary between Phenobarbital and Potassium Bromide
Phenobarbital: 10-14 days (half life 24 hrs)
Potassium Bromide: 100-200 days (half life 14 days)
When should plasma levels of a) KBr and b) Phenobarbital be taken
a) KBr: 4 weeks
b) Phenobar: 14 days
How does excretion route vary between phenobarb and KBr
Phenobarb: Liver metabolised (hence common increase in aLP/ Hepatotoxicity)
KBr: Renal excretion
Seizures are normally the result of involvement of the __-
Forebrain involvement
can be caused by extracraninal causes e.g. metabolic
What diet can influence serum concentration of Potassium Bromide?
High chloride in the diet can lower serum concentration of Potassium Bromide
What toxicity is associated with KBr?
How is it treated?
RARE.
Severe ataxia, sedation, skin reaction.
Normally due to renal insufficiency (as renally excreted c.f. phenobarb = liver)
THERAPY = IV FLUIDS TO INCREASE EXCRETION
Which seizure therapy does not require serum drug monitoring?
Imepitoin,
Not recommended for status epilepticus or cluster seizures in cats.
Only licenced for idiopathic epilepsy in dogs
Therapeutic index for Imepitoin
No ideosyncreatic reactions have been observed.
Drugs appears safe with good therapeutic index..
NO EFFECT ON LIVER ENZYMES
When is Imepitoin indicated
First line treatment for dogs with newly diagnosed idiopathic epilepsy (no serum monitoring required).
NOT for cluster seizures/ status epilepticus or in cats
Good for patients that have side effects on phenobarb.
Patients can develop tolerance to which antiepilpetic drug
Phenobarb/
A ‘non-responder’ to anti-epilepsy medication is a patient whose seizure frequency doesn’t reduce below ___ %
Below 50% reduction in seizure frequency = failure.
2 add on drugs for refractory seizures and there side effects
- Gabapentin - sedation ataxia
2. Levetiracetam - Sedation (rare)
First and second choice AED’s for cats
- Phenobarb (polyphag, bone marrow suppression, cutaneous hypersensitivity)
- Diazepam (hepatotoxicity- contraindic in liver disease)
Diazepam can’t be used in dogs as develop tolerance.
Why is KBr not used in cats with epilepsy
Bronchial asthma
Status epilepticus up to 30 minutes leads to
Stress response: Arterial hypertension, Increased cerebral blood flow, Hypoxemia, Hypercarbaemia, HYPERglycemia, lactic acidosis
Status epilepticus >30 minutes leads to
Continous muscle contraction. Hyperthermia, Acidosis, Myolysis- hyperkalemia- renal failure.
HYPOglycemia
Hypotension
Cardiac arrthymias
Post status epilepticus considerations
minimise brian injury., Treat hypotension - supplement O2.. Treat hypotension, volume expansion.
Monitor electrolytes.
Minimise hyperthermia./ renal impairment
TREAT UNDERLYING DISEASE
- Hypoglycemia? Toxicity?? - DIURESIS
Ataxia is divided into what 3 types
- Sensory
- Vestibular
- Cerebellar
Clinical signs of Sensory ataxia
Abnormal postural reactions. Limb paresis - knuckling.
Wide based stance/ increased stride length.
Clinical signs of Vestibular ataxia
Heat tilt, learning, falling or rolling to one side. Abnormal nystagmus. NORMALLY TILT TOWARDS SIDE OF LESION
Clinical signs of Cerebellar ataxia
Cerebellum fine tunes movement
- Wide based stance, intention tremors of the head. Loss of balance/truncal sway
A wide based stance is indicative of ___ ataxia
Cerebellar ataxia. Wide based stance Intention trmors of the head. Loss of balance and truncal sway. Ipsilateral meance defects with normal vision (II-->Forebrain-->Cerebellum--> Brainstem--> VII
Which breed of cat has a congenital nystgamus>
Siamese
Ptosis is
‘drooping’ or falling of the eyelid. Clinical sign of Horners syndrome alone with Enophtalmos (posterior displacement of globe into orbit)
Additional clinical sign of Horner’s syndrome in horse
- Ptsosis (drooping of eyelid)
- miosis
- Enophtalmus (posterior displacement of globe)
- Prominant third eyelid
- Conjunctival/Nasal hyperaemia
- SWEATING!! See regional sweating pattern, follows symph
Function of the Saccule and Urticule
Head position/gravity.
Semicircular canals = head motion/ angular acceleration.
Cerebellum is primarily ______ to vestibular nuceli
Cerebellum is primarily INHIBITORY to vestibular nuclei.
Signs of cerebellar ataxia: Wide base stance, intention tremors of the head, ipsilateral menace deficits with normal vision
A rotary jerk nystagmus can’t be seen in what species?
Can’t be seen in dogs as pupil is round.
How can CENTRAL vestibular and PERIPHERAL vestibular disease be differentiated
Rotary/Horizontal nystagmus can be either central/peripheral.
Vertical Nystagmus can only be central vestbular.
Horners syndrome is more likely to be CENTRAL/PERIPHERAL vestibular?
More likely to be peripheral vestibular.
Rare for horners syndrome to be caused by central.
Vertical nystagmus is CENTRAL/PERIPHERAL VESTIBULAR DISEASE?
Vertical nystagmus = Central vestibular.
Which cranial nerves affected in a) central b) peripheral vestibular disease
a) central. CN V-XII
b) Peipheral: CN VII only
Peripheral vestibular disease STEP 1 is to determine if…
Ototoxic drugs have been given. If given, STOP.
If not given- otoscopic examination. Check if otitis media, interna or neoplasia.
Myringtotomy
Rostral lobe cerebellar ataxia
Decerebellate posture (optistontonus, forelimb hyperextention, hindlimb flexion))
Hypermetria and Intention tremor is indicitive of ____ataxia
Caudal lobe Cerebellar ataxia
What would you expect if the Flocculonodular lobe was affected by cerebellar ataxia
Dysequilibrium. Broad based gait
Paradoxical vestibular signs are expected when which part of cerebellum is damaged
Caudal cerebellar peduncle = cerebellar ataxia.
With paradoxical vestibular = HEAD TILT IS OPPOSITE to SITE of lesion,
With central vestibular= HEAD TILT IS SAME SIDE AS LESION
The reticular activating system is a network of nerves with pathways to the ___
forebrain
Ddx of Mentation changes causes by neurological disorder
Changes in mentation can be due to neurological disorders but can also be due to systemic disorder e.g. pyrexia/ hypertension
Forebrain is divided into what 3 areas
- Association area- Cerebral cortex- Neocortex
- Emotion area- Limbic systemic - Archicortex
- Olfactory area- Olfactory bulb (Paleocortex)
The limbic system is
The second part of the forebr5ain - emotion area- archicortex
Pleurothotonus is
head turn/ turning of the body
Forebrain syndrome includes
- Altered mentation
- Pacing/ Head pressing/ Pleurothotonus
- Decreased/ absent menace response with normal PLR (see pathway)
- Deficits to contralateral limb
- Normal/increasd reflexes in contralateral limb
Muscle tone can be increased.
Cranial nerves exiting the brainstem include
III-XII. Also contains vestibular system
Brainstem syndrome
Paresis- all 4 limbs, or ipsilateral), opisthotonus, Decerebrate posture (posit, extension all4 limbs)
Spinal reflexes normal to increased in all OR IPSILATERAL limbs (c.f. forebrain syndrome)
Decreased sensation (face)
Pacing/ head pressing is indicative of
Forebrain syndrome.
Altered meance response/ normal PLR.
Increased/normal spinal reflxes and muscle tone in contralateral limb.
c.f. brainstem syndrome= ipsilateral
From what age is the menace reponse present
Cortical response.
From 12 weeks old.
A medial strabismus would be indicative of damage to which nerve/
Abducens = innervates Lateral rectus therefore damage to this would lead to medial strabismus
Sensory innervation to the a) medial canthus of eye b) lateral canthus of eye
a) medial = ophthalmic branch
b) lateral = maxillary branch
Of trigem
Sensory ‘taste’ to Rostral 2/3rds of tongue is suppled by
taste to the rostral 2/3rd of the tongue is fungiform papillae which are innervated by facial nerve (chorda tympani branch),
Sensoneural deafness is linked to
White coat and blue eyes. e.g. merle gene.
Dalmation.
Hiar cells die at 3-4 weeks.
Most common cause of Sensoineureal deafness is Otitis Interna
3 causes of Conductive deafness
Neoplasia, Infection (otitis media) inflamm (polyp in cats)
Larangeal sensation and Larynx / Pharynx motor supplied by
Vagus X
Inspiratory dysnoea, most likely cause
Vagus brances to recurrent larangeal nerve.
4 causes of Acquired Megaoesophagus
CARE ASPIRATION PNEUMONA
- Hypoadrenocorticoism (addisions)
- Myasehtesia Gravis
- Oesophagitis
- Botulism
- BRAINSTEM DISEASE
What would be the effect on a) vision b) menace c) PLR of a lesion at the optic chiasm
NO VISION, NO MENACE AND NO PLR BILATERALLY
Treatment for Permetherin toxicity
Decontaminate bath - WARM, TOOHOT may increase absorption.
Activated charcoal.
Duazepam/ Propofol infusion.
Cerebral hypoplasia in a calve most likely due to
BVDV - Pestivirus (RNA)
Same as border disease in lambs ‘hairy shaker lamb’
Cerebellar hypoplasia in a kitten with voming, dirrhoea and reduced white blood cells most likely
Feline panleukopenia virus (cat equiv of parvo BUT parvo has no cerebellar hypoplasia)
2 diseases that cause cerebellar hypoplasia in calves
Smallenberg, blue tongue, BVDV
Horse spinal cord with haemorrhage/ infarct/ necrosis ‘spheroids’ - likely virus?
EHV-1 respiratory and neurological.
EHV-1 pathogenesis of neurological signs
Only effects spinal cord. Attacks endothelium causes arteritis. Thrombus causes necrosis - infarction of axons- respond by swelling forming ‘ spheroids’
Diagnosis of EHV-1
CSF tap.
ISOLATE HORSES. Don’t move on to or off yard
Type of virus that causes FIP.
How does it causes CNS signs?
Cornavirus Dry form causes granulomatous lesions.
Wet form = effusion’
Piglet with nystagum, paddling movement of the limbs. Necrospy reveals widespread haemorrgage and prulent exudate / meningitis. Likely pathogen =
Strep suis.
Extensors stronger than flexors. Less inhibition from UMN.
