Dogs and cats 25 Flashcards
brainstem syndrome which side are signs and the main structures and therefore functions affected - EXAM
IPSILATERAL SIGNS
Main structures and functions affected - IMPORTANT
- Mainly white matter similar to the spinal cord
- Proprioceptive tracts (13) - proprioception
- Motor tracts (15) - voluntary motor function
- Ascending reticular activating system (16) - arousal (KEEPS YOU AWAKE)
- Nuclei of the cranial nerves (6, 7, 8, 9) - cranial nerves
- Cardiorespiratory centres - life
Neurological examination what seen with brainstem syndrome
- Observation - from all functions
○ Decreased mental status - reticular activating system
○ Four limb ataxia/paresis
○ Vestibular ataxia - Palpation - normal
- Postural reactions - decreased (proprioception decreased)
- Spinal reflexes an tone - normal
- Cranial nerves - affected (expect cranial nerve 2)
- Sensory systems - normal
○ UNLESS COMA
Where is the lesion?
1) If head tilt to left AND proprioception decreased on LEFT
2) If head tilt to the right AND proprioception decreased on LEFT
1) left brainstem
2) right forebrain
What are the 2 main things that result from brainstem and forebrain syndrome and the clinical signs
- Cushing reflex
a. brain lesion -> increase intracranial pressure
b. Increase systemic blood pressure (BP) to increase cerebral blood flow
c. Decrease heart rate if baroreflex works - Cushing triad
○ Brain signs (shallow breathing) - IMPORTANT
○ High BP
○ Low HR
cerebellar syndrome what side are the signs and the main function
IPSILATERAL SIGNS
Functions of the cerebellum
- “Coordination of movements so they are fluid in nature” Sean
Neurological examination what seen with cerebellar syndrome
- Observation
○ Cerebellar ataxia
§ Wide based stance
§ Hypermetria - exaggerated movements (lifting the legs higher than needed)
○ Intention tremors - worse when intending to do something - Palpation - normal
- Postural reactions - normal
- Spinal reflexes and tone - normal
- Cranial nerves
○ Normal or decreased
§ No menace response if severe - ipsilateral
□ Response as involves the forebrain (conscious)
□ relay in the cerebellum - SAME SIDE AS STIMULATED
§ Anisocoria - rare
□ Ipsilateral mydriasis
□ Slowly responsive to light
□ Fastigial and/or interpositus nuclei - Sensory systems – normal
Encephalpathies what are the 7 main ones
1) cerebellar abiotrophy
2) hydrocephalus
3) brain tumours
4) thiamine deficiency
5) Meningoencephalitides of unknown origin (MUO)
6) Steroid-responsive-tremor-syndrome
7) Cerebro-vascular accidents (stroke)
Cerebellar abiotrophy what is it, cause and clinical signs
- Degeneration of normal neurons after birth
- Cause
○ Unknown
○ Some reclassified: storage disease
§ Am. Staffordshire terrier - Genetic
○ Aus. Kelpie, Border Colley, Brittany spaniel… - Clinical signs = cerebellar
○ Progressive (slow or quick)
○ Adult (but early or late)
○ Plateaus
Cerebellar abiotrphy diagnosis, treatment and prognosis
- Diagnosis ○ Strong clinical suspicion ○ MRI when advanced ○ Genetic tests (breed specific) - No treatment - Prognosis - can still be alive at 12-13 years of age, other may deteriorate
Hydrocephalus cause, breeds, cliical signs
- Congenital - almost always ○ Likely obstructive ○ No cause on presentation - Small breed dogs - pugs, Pekinese - Clinical signs ○ First sight… § Dome shaped head, open fontanelles, “sunset eyes” - bulging out ○ Neurological § Forebrain - variable § Slow to train, central blindness (compress occipital lobe), obtundation, pacing § Seizures <20%
Hydrocephalus diagnosis and treatment
- Diagnosis
○ U/S, CT-scan, MRI - Treatment
○ When? - no real indications - some plateau and some get worse
○ Help reduce CSF formation and increase drainage
○ Medical - corticosteroids (increase drainage)
○ Surgical; Ventriculo-peritoneal shunt
Brain tumours what are most common in dog and cat, primary or secondary and clinical signs
- Dog ○ Primary -> meningioma, astrocytoma, oligoendrogiloma, glioblastoma, lymphoma ○ Secondary -> haemangiosarcoma, pituitary adenoma/carcinoma, lymphoma, nasal tumours - Cats ○ Meningioma, gliomas, ependymoma, other primary, lymphoma - Primary > secondary - Older individuals - Clinical signs ○ Depends on location § Forebrain > … § Seizures in <25% cats ○ Acute to slowly progressive
Brain tumours diagnosis
○ MRI
§ Sensitive, accurate
§ Often characteristic…
□ Meningiomas (grow from the meninges, strong uptake on contrast on tumour and peri-tumoral oedema around the tumour)
□ Gliomas (within the parenchmya - harder to remove surgically)
□ choroid plexus tumours - highly vascular and produce the CSF
§ …but not always - Lymphomas
○ CT-scan
§ Approx. 20% less sensitive and harder to describe the tumours
○ Skull radiographs
○ CSF - non specific
○ Brain biopsy - not common
Brain tumours staging how common metastasis and which hard to treat with chemotherpy
○ Malignant and brain tumours
§ Metastasis, cytology, local behaviour
○ 23% of dogs have a tumour somewhere else that is unrelated! - due to the age as likely to have other tumours NOT that the brain tumours metastasise (don’t do this that commonly)
§ Important to know this before surgery
○ Lymphoma - hard to treat with chemotherapy
§ FeLV, thorax-abdomen, bone marrow
Brain tumours treatment which treat, which has best prognosis and options
○ Primary > secondary (no as metastases - worse prognosis)
○ Meningioma (best prognosis and generally more accessible) > others
○ Palliative
§ Steroids +/- anticonvulsants
§ MST ≈ 2 months
○ Chemotherapy
○ Surgery - brain surgery - WILL GROW BACK
§ MST ≈ 18 months
○ Radiation therapy (megavoltage)
§ MST ≈ 10 to 100 weeks
Thiamine deficiency how does it lead to an encephalopathy and clinical signs
○ Thiamine = vitamin B1 – CoE § Energy (Krebs cycle) § Production of acetylcholine and GABA Deficiency -> Polioencephalomalacia = Lack of grey matter (has high metabolic requirement, highly sensitive) - Clinical signs ○ Central vestibular syndrome § Bilateral vestibular syndrome § Neck ventroflexion § Facial paralysis § Abnormal PLRs § Ataxia ○ Forebrain § Decreased mental status § Seizures § Central blindness
Thiamine deficiency diagnosis, treatment and prognosis
- Diagnosis ○ MRI – pathognomonic images - symmetry of the lesions in the grey matter ○ Complicated otherwise § [Thiamine] food, erythrocytes - Treatment ○ Thiamine supplementation - Good prognosis - Might take a while
Meningoencephalitides of unknown origin (MUO) define, what are the types and cause
- Definitions
○ Inflammatory non-infectious (MUCH MORE COMMON)»_space;> infectious (rare)
○ Various histo types
§ GME = Granulomatous Meningo-Encephalitis - most common
§ NME = Necrotizing Meningo-Encephalitis
§ NLE = Necrotizing Leuko-Encephalitis
→ Meningo-encephalitis of Unknown Origin (MUO) - Aetiology? - unsure but some genetics as breed specific
○ Same breeds, young adults
Meningoencephalitides of unknown origin (MUO) clinical signs and diagnosis
Clinical signs ○ Depending on location ○ Multifocal! ○ Optic neuritis → acute blindness ○ Spinal forms, neck pain Diagnosis a. MRI >> CT - ensure there is something in the brain b. CSF tap – meningitis § Non-specific mononuclear pleyocytosis c. Rule out infectious diseases - as using immunosuppressive drugs § PCR on CSF § Serology N. caninum, C. neoformans, distemper
Meningoencephalitides of unknown origin (MUO) treatment and prognosis
- Treatment ○ Prednisolone (immunosuppressive) § Then tapered down ○ + cyclosporine, azathioprine, cytarabine ○ Follow up crucial § Clinical § Repeat MRI, CSF? - Prognosis ○ MST ≈ 300 to 1500 days ○ Importance of short term survival
Cerebro-vascular accidents (stroke) types, cause and clinical signs - EXAM
- Types -> Ischaemic (Artery blockage)»_space;> haemorrhagic (Artery leaking)
- Causes
○ Unknown > 50%
○ Hypertension, hypothyroidism, hyperadrenocorticism… - Abrupt clinical signs - neuromuscular defects -> head tilt, turn
○ Sometimes progression over 48h (oedema)
○ Raised ICP if haemorrhagic
Cerebro-vascular accidents (stroke) diagnosis, what should look for and prognosis
- MRI diagnosis - helps you to find where the accident is: ○ Diffusion Weighted Images (DWI) ○ Gradient Echo (T2*) - Underlying cause ○ Not found in 50% of cases § Coagulopathies § Hypertension § Endocrine diseases § Cardiac diseases/hypertension - Good prognosis - usually recover within 2-3 weeks
Vestibular systems structures and other structures associated with
- Receptors / internal ear - near facial nerve
- Vestibular nerve / petrous bone
- Vestibular nuclei / brainstem
○ Spinal cord
§ Vestibulospinal tract -> maintain balance of the body
○ Brain stem
§ Medial longitudinal formation (MLF) - coordination of eye movements when moving
§ Reticular formation -> arousal -> when going to fall over you wake up
§ Vomiting centre
§ Thalamus - conscious integration
§ Cerebellum - movement coordination
What is the normal functioning of vestibular system and what occurs when things go wrong
- Body balance in response to gravity using Head and eyeballs
○ NORMAL - If going to fall to the left the vestibular system stimulation of ipsilateral extensor muscles (left) and inhibition of contralateral extensor muscles -> then correct positioning back into neutral position
○ ABNORMAL (lesion on left) - losing stimulation of ipsilateral extensor muscles on the left -> so falls over towards the left
In terms of neurological examination what found on observation and why
1) Vestibular ataxia
1. Circling/falling - to the side of the lesion
□ Ipsilateral increase flexion (due to decreased extension)
□ Contralateral increase extension
2. Head tilt
□ Same reason as circling (ipsilateral increase flexion)
□ Scoliosis with neck/trunk turned to the side of the lesion
3. Nystagmus - involuntary, rhythmic oscillation of the eyes
□ Same reasons as above
□ Generally involved both eyes
□ Sudden attempt to re-adjust the axis of the eyeball
® Quick phase opposite to the lesion
□ ALSO
® Horizontal vs rotatory vs vertical
® Positional nystagmus
◊ Absent/abnormal oculo-vestibular reflex (aka oculocephalic or physiological nystagmus)
2) Strabismus
§ Misalignment of the eyes - not as common
§ “Vestibular strabismus”
□ As moving head up Eye on the side of the lesion may struggle to move up and remain in ventro-lateral position
Vestibular disease neurological exam findings all besides observation
- Palpation - normal
- Postural reactions - normal to abnormal
- Spinal reflexes and tone - normal
- Cranial nerves - abnormal
○ Absent oculo-vestibular reflex
○ Resting (pathological nystagmus)
○ Positional nystagmus - vertical nystagmus indicates central vestibular syndrome
○ Positional strabismus - Sensory systems - normal
What are the 2 main types of vestibular syndromes and what associated with
- Peripheral - lesion in the ear (facial nerve is associated with the ear)
- Central - lesion in the brain stem (have proprioception tracts within, motor pathways and reticular foramen)
What are the 3 main causes of peripheral vestibular syndrome
1) Infectious otitis media-interna - MOST COMMON CAUSE
2) Idiopathic/geriatric vestibular syndrome - second more common
3) Primary secretory otitis media-interna (PSOM)
What is the most common cause of peripheral vestibular disease, pathophysiology, clinical signs and diagnosis
Infectious otitis media-interna - Physiopathology ○ Often otitis externa § Staphylococcus spp. Streptococcus spp. ○ Underlying causes § Atopy, foreign bodies… - Clinical signs ○ Peripheral vestibular syndrome ○ +/- facial paralysis ○ +/- Horner syndrome ○ Deafness? - Diagnosis ○ Otoscopic examination § Cytological examination ○ Imaging § Radiographs
Infectious otitis media-interna treatment and prognosis
- Treatment and prognosis ○ Topical treatment ○ Systemic antibiotics - recommended § Based on culture and sensitivity § Cephalexin, Amoxicillin ○ Myringotomy, bulla osteotomy - need to drain the puss out ○ Addressing underlying condition-atopy - Guarded to fair prognosis ○ Depending if brain extension
Idiopathic/geriatric vestibular syndrome pathophysiology, clinical signs, diagnosis, treatment and prognosis
- Physiopathology ○ Unknown – thickening of endolymph? ○ Older dogs – adult cats - Clinical signs ○ Peripheral vestibular syndrome ○ Hyperacute, marked (struggle to work and very imbalanced) - Diagnosis ○ Exclusion - Treatment and prognosis ○ No treatment just time ○ Diazepam 0.5mg/kg TID – motion sickness - Good prognosis – 2 weeks
Primary secretory otitis media-interna (PSOM) what a cause of, what is involved, main breed, clinical signs, treatment and prognosis
peripheral vestibular disease - Viscous mucus plug ○ Abnormal Eustachian tube ○ Non-infectious at first - Cavalier KCS - Clinical signs ○ Head and neck discomfort ○ Peripheral vestibular signs § +/- Horner and facial paresis - Myringotomy, flush - Good prognosis
Define a seizure
○ brain disorder expressed as a paroxysmal transitory disturbance of brain function that has:
§ a sudden onset,
§ ceases spontaneously,
§ has a tendency to recur,
originates in the prosencephalon (Delahunta)
Seizure what is the main characteristic, clinical signs and what are the 4 phases
○ Main characteristics § Loss of control § Episodic (paroxysmal) - back to normal straight after episode § Repetitive clinical pattern ○ Clinical signs § Consciousness § Motor § Sensory - hard to detect § Autonomic § Psychic - hard to detect Phases a. Pre-ictal = prodromes b. Aura (short) c. Ictus - seizure itself (burst of motor activity) d. Post-ictal § Cerebral exhaustion
How does a seizure occur and the 2 main types
○ Every neuron has a seizure threshold
○ Imbalance: Excitatory-inhibitory impulses altered:
§ Synapses (dendrites) - brain lesions
§ Cell membrane - brain lesions
□ Genetics (lipoproteins, channels…)
§ Neurotransmitters - idiopathic/familial
□ Inhibitory: GABA
□ Excitatory: glutamate
§ Environment - metabolic
□ Glucose, electrolytes
Types
1) generalised - origin from both forebrain hemispheres
2) partial - one focus lesion in the forebrain
Generalised seizure origin and presentation
origin from both forebrain hemispheres § Primary generalised § Presentation □ Motor signs = convulsion ® Tonic-clonic (tonic - rigid, clonic - uncontrolled extension/jerking) □ + loss of consciousness □ +/- autonomic, psychic, sensory ® Autonomic = salivation, change in pupils size, urination, defecation… □ Psychic and sensory: hard to tell…
Partial seizure origin, presentation and types within
origin from both forebrain hemispheres § Primary generalised § Presentation □ Motor signs = convulsion ® Tonic-clonic (tonic - rigid, clonic - uncontrolled extension/jerking) □ + loss of consciousness □ +/- autonomic, psychic, sensory ® Autonomic = salivation, change in pupils size, urination, defecation… □ Psychic and sensory: hard to tell…
What are some common presentations (pheonotypes) of partial seizures
§ Facial twitching (simple motor)
§ Other localised motor
□ tonic of one leg +/- trunk +/- neck (simple motor)
§ Hypersyalosis + oral involvement (simple autonomic)
§ Fly biting (simple sensory) - form of hallucination
NOT head bobbing
What are the 3 differential type of seizures in terms of duration and frequency and what is epilepsy
1) Isolated § One seizure or less / day 2) Cluster § Two seizures or more / day 3) Status epilepticus § Two seizures within 30 minutes without recovery § One seizure > 5 minutes duration Epilepsy - Greek epilepsia = to be taken - Recurrent seizures = 2 or more in the life Regardless of the origin! - - DOESN'T INDENTIFY THE CAUSE
What are the 3 main types of seizures that help narrow down differentials
1) extra-cranial
2) intra-cranial
3) idiopathic (familial)
