Week 2-3 - Neuro Flashcards
Contraindications of KBr for seizure management (3)
- Renal dz (b/c KBr is eliminated via the kidneys)
- Hx of pancreatitis (since KBr can cause pancreatitis in dogs)
- Rapid control of seizures needed (b/c KBr has a long elimination half life at ~24 days, so it reaches steady state at 3-4 months
Zonisamide - adverse effects: (6)
- Sedation and ataxia - self-limiting within first two weeks of therapy, worse in large breeds
- GI upset - hyperemia, v/d
- Immune-mediated keratoconjuncitvitis sicca (KCS), polyarthropathy (b/c sulfonamide derivative)
- Renal tubular acidosis (b/c sulfonamide derivative)
- Decreased T4
- Acute hepatic necrosis (rare)
Zonisamide - contraindications: (1)
- Pre-existing keratoconjuncitivitis
Levetiracetam - metabolism:
-70-90% excreted in urine (bioavailability is nearly 100%)
Levetiracetam - adverse effects (2):
- Sedation and ataxia
- Anorexia in cats
usually uncommon
Levetiracetam - contraindications: (1)
- Poor efficacy as a monotherapy for epilepsy (EXCEPT for feline audiogenic reflex seizure)
Levetiracetam – what does the honeymoon period refer to?
Honeymoon period – great response to drugs in the beginning, then fades away
What is refractory epilepsy?
When there is a failure of adequate trails of two tolerate, appropriately used anti-epileptic drugs (AEDs)
When should a second AED be added? (4)
ACVIM Panel recommends:
1. appropriate drugs and maximal level of first AED for a minimum of 3mo
2. >50% increase in seizure frequency over 3mo
3. new onset of status epilecticus or cluster seizures
4. present of drug toxicity
When do we start AED (anti-epileptic drug) therapy? (4)
- identifiable structural lesion OR hx of encephalopathy/trauma
- acute, repetitive seizures (3 or more generalized seizures in 24 hrs, status epilecticus)
- 2 or more seizure events within 6 months
- prolonged, severe, or unusual post-ictal period
What diagnostics should you recommend for a seizing patient? (4)
- minimum database (CBC, chem, UA, 3-view thoracic rads, abdominal US)
- intracranial imaging (MRI - gold standard)
- CSF analysis
- EEG
When are seizures considered an EMERGENCY? (3)
- status epilecticus
a. ictus 5 min or more
b. 2 or more seizures without regaining consciousness - cluster seizures (3 or more generalized seizures within 24 hours)
- failure to regain consciousness within 1-2 hours of ictus
Status epilecticus risks: (2)
- intoxication (bromethelin, caffeine, chocolate, etc. – toxins in the CNS)
- idiopathic epilepsy
Status epilecticus: How does Ca2+ contribute to primary brain injury?
NEURONAL DEATH via excitatory neurotoxicity –> an influx of Ca2+ is BAD – it causes cells to apoptose, adds oxidative stress, causes dendritic remodeling, inflammation, and necrosis
Status epilecticus: How/why does cerebral edema contribute to primary brain injury?
during a seizure, higher metabolic demands increases cerebral blood flow (200%-700%)
- hyperperfusion – BBB disruption
- if metabolic demands are not med, then LACTATE is made – BBB disruption
The 2 Phases of Status Epilecticus
Phase I: Compensated status epilecticus
-increase in autonomic activity
-elevated catecholamines, endogenous steroids
-hypertension, tachycardia, hyperglycemia, hyperthermia, ptyalism (drooling)
-temperature will increase
Phase II: Uncompensated status epilecticus
-~30 min following continuous ictus – cerebrovascular auto regulation fails, ICP rises
-hypotension, hypoglycemia, hyperthermia, hypoxia
…ultimately leading to:
-respiratory failure
-metabolic acidosis
-hyponatremia
-hyperkalemia
RISK FOR SUDDEN DEATH
Systemic effects of Status Epilecticus (3)
- Kidneys: poor perfusion + muscle death –> lead to acute renal failure
- Skeletal muscle: death of muscle secondary to hyperthermia
- Heart: arrhythmias
Convulsive status epilecticus (CSE) characteristics: (3)
- generalized tonic/clonic movements
- impaired consciousness
- +/- autonomic manifestations
majority of dogs/cats
Non-convulsive status epilecticus (NCSE) characteristics: (3)
- EEG evidence of seizure activity without clinical appearance associated with CSE
- may occur before or after convulsive seizures are present
- could be for patient with prolonged period of impaired consciousness following CSE tx
EEG necessary to rule out NCSE
Goals of seizure treatment/status epilecticus: (4)
- stop the seizure
- prevent further seizures
- manage seizure complications
- manage underlying conditions causing seizures
Which 1st line anti-epileptic drug should be administered in an emergency? (2)
BENZODIAZEPINES
- Diazepam: IV (0.5mg/kg) or per rectum (1-2mg/kg)
- Midazolam: IV or IN (0.2-0.5mg/kg)
midaz>diaz, midaz more favorable
20lb dog = 0.5mL midazolam IV/IN; 1mL diazepam IV
What other aspects should you consider when trying to STOP THE SEIZURE (emergency setting)? (5)
- establish IVC access
- check electrolytes
- supply flow-by O2, bc PaO2 <50 increases ICP (and we don’t want increased ICP)
- if hyperthermic, cool down! (stopping seizure will help this)
- blood pressure - if elevated ICP, reduce it (hypertonic saline, mannitol, keep head elevated over 30 degrees)
I’ve given 2-3 benzodiazepine boluses and started CRI AND loaded with a a long-acting AED. Patient is still seizing. Now what?
Patient is refractory!
- Propofol – GABAa receptor agonist/inhibits NMDA receptors
-modulates slow Ca2+ ion channels
-administer as CRI bc half life is very short - IF STILL SEIZING – add inhalant anesthetic gases
-iso/sevo - GABAa recepter agonists
What is Cushing’s Reflex?
It’s a reflex in response to increased ICP. Increased ICP decreases cerebral blood flow, so ischemia occurs. Ischemia causes systemic hypertension (increases mean arterial pressure) to try and improve blood flow. Baroreceptors sense the increased MAP and have a reflex bradycardia.
Ultimately results in
-increased systolic BP
-low HR
-low RR (?)
Trigeminal nerve is which CN? What are its branches?
CNV
a. opthalmic - (sensory)
b. maxillary (sensory)
c. mandibular (motor - for mastication, sensory)
Mandibular nerve exits the skull through _____ foramen.
OVAL foramen
What are the muscles of mastication? (3)
There are 5, but the ones we should know are:
- masseter
- termporalis
- pterygoids
All sensory axons for CNV enter the _______ ___ ___ ____.
brainstem at the pons
CNV Testing: Cutaneous Sensation methods: (4)
- Corneal reflex: moist Q-tip, gently touch cornea, observe retraction of globe/eye blink
-afferent: CNVa (ophthalmic)
-efferent: CNVI +/- CNVII - Palbebral reflex: touch lateral and medial canthus of eyes, observe eye blink
-afferent: CNVa and CNVb (ophthalmic and maxillary)
-efferent: CNVII - Trigeminofacial reflex: Touch area of maxillary vibrissae, observe for eye blink
-afferent: CNV (ophthalmic and maxillary)
-efferent: CNVII - Noxious responses:
-requires cortical processing (not just reflex)
-afferent: CNV
-blunt stimulation of nasal mucosa (CNVa and CNVb)
-Noxious stimulus to the lateral maxilla at the level of the canine tooth (CNVb –> lead to efferent CNVII)
-Noxious stimulus to the lateral mandible at the level of the canine tooth (CNVc –> lead to efferent CNVII)
CNV Testing: Motor Function: (3)
- paresis/paralysis: ability to close mouth and pretend food, difficult to see if unilateral
- atrophy: mastication muscles, eyes may be sunken in due to atrophy of pterygoid m.
- symmetry and tone
Clinical signs of CNV Dysfunction (Sensory, 6 and Motor, 3)
SENSORY Dysfunction:
1. decreased sensation (hypesthesia, anesthesia)
2. decreased or absent reflexes (palpebral, corneal, trigeminofacial)
3. reduced facial sensation
4. corneal ulcer
5. abnormal (paresthesia, hyperesthesia)
6. rubbing or pawing at face
MOTOR Dysfunction
1. masticatory muscle paresis or paralysis
-unilateral—difficult to detect clinically
-bilateral—dropped jaw, inability to close mouth, drooling, difficulty in prehending food
2. masticatory muscle atrophy (masseter, temporalis, pterygoids)
-severe neurogenic atrophy (unilateral or bilateral), “caved in head”
3. trismus (difficulty opening mouth)
Localizing a CNV lesion (2)
- Intracranial: brainstem - pons and rostral medulla
-motor and sensory dysfunction
-brainstem signs:
-CN deficits, esp CNVII and CNVIII
-ipsilateral hemiparesis
-obtundation
-CP deficits
-cerebellar signs - Extracranial
-signs vary
-NO brainstem signs
How to diagnose a CNV lesion?
- hx
- clinical signs
- advanced imaging (MRI preferred over CT)
- CSF analysis
- +/- skull radiographs
- for dogs: +/- type 2M antibody serology (for masticory muscle myositis - MMM)
CNV Disease: Idiopathic Trigeminal Neuropathy
IDIOPATHIC: Idiopathic Trigeminal Neuropathy
-aka trigeminal neuritis
-don’t know underlying dz
-common in dogs, uncommon in cats
-ACUTE onset - dropped jaw, inability to close mouth
-dysphagia, drooling
-sensation usually normal
-atrophy common, may be unilateral
-+/- Horner’s syndrome, facial paralysis associated
DIAGNOSIS
-hx, clinical signs
-negative serology for type 2M antibody (rule out MMM)
-MRI + CSF (may see enhancement of trigeminal nerve(s) and masticatory muscle atrophy on MRI)
-diagnosis of exclusion
-electrophysiology and muscle biopsy (not common), biopsy difficult
TX
-supportive care - tube feeding, fluids
-corticosteroids NOT recommended
PROGNOSIS
-usually resolves within 2-6 weeks
RULE OUT DDX:
-Masticatory muscle myositis (MMM) – usually don’t have dropped jaw though, usually have trismus, not unilateral, may have muscle swelling or pain
-neoplasia: lymphoma, round cell neoplasia
-infection: rabies
-trauma
CNV Disease: Infection: Rabies
-predilection for brainstem: most common clinical signs:
-pharyngeal paralysis: (nucleus ambiguous (CN IX and X))
-dropped jaw (motor nucleus of CN V)
-clinical signs are progressive once neurological signs are apparent
-obtain a thorough history from ALL animals with a hx of DROPPED JAW, including
vaccination history, and environment (re: exposure) history, remember, this is a zoonotic
disease
-incubation: 7 days to 1 year
-recovery rare once CS develop
CNV Disease: Neoplasia and Trauma
NEOPLASIA
- intracranial
-primary and secondary neoplasia - extramedullary
-lymphoma
-malignant peripheral nerve sheath tumor
-squamous cell carcinoma and parotid adenocarcinoma.
-a good minimum database is important. Prognosis generally poor but varies with type of neoplasia.
TRAUMA
-signs are acute, and other cranial nerves such as the facial nerve, may also be involved
-resolution of signs depends on the severity of the injury
CNVII Functions
-motor: facial expression
-sensory: concave surface of skin on pinna
-taste to rostral 2/3 of tongue
-parasympathetic fibers to lacrimal and salivary glands
CNVII and CNVIII exits brainstem at _____ _______ _______
INTERNAL ACOUSTIC MEATUS
CNVII exits the skull at the _______ foramen.
Stylomastoid
CNVII Testing - Which reflexes? (4)
- Menace (A: CNII, E: CNVII)
- Corneal (A: CNVa, E: CNVII)
- Palpebral (A: CNVa/b, E: CNVII)
- Trigeminofacial (A: CNVa/b, E: CNVII)
CNVII Motor Dysfunction
-inability to close eye
-dropping ear, eyelid, lip
-widening of palpebral fissure
-NO nostral flare
-facial spare (rare)
CNVII Sensory Dysfunction
-impaired taste
-reduced or absent sensation on medial surface of pinna
-hyperacusis (hypersensitivity to normal sound)
What is CNVII’s parasympathetic function? How does an autonomic dysfunction of CNVII present?
-Lacrimation (Schirmer tear test)
-presents as dry eye and nose – can lead to corneal ulcers
Localization of CNVII lesions?
- Intracranial - brainstem
-motor, sensory, and parasympathetic involved
-ipsilateral CNVII paresis/paralysis
-reduced/absent lacrimation, taste
-other brainstem signs (obtundation, CP deficits, etc)
INTEROSSEOUS NERVE
CN VII paresis/paralysis (reduced to absent reflexes)
-No brainstem signs
-+/-taste sensation
-+/-lacrimation
-CN VIII signs +/-
-Signs of middle ear disease may be present (+/- vestibular signs, signs of Horner’s syndrome)
- Extracranial
-CS depend on localization of lesion along nerve
-NORMAL lacrimation and taste
CNVII Diagnosis plan
-CS
-hx, PE, NE
-Schirmer tear test, taste test
-electrodiagnostics (BAER to evaluate CNVIII, EMG, NCV) - not common
-MRI + CT
-skull rads
-CSF analysis
-otoscopic exam
Ddx of CNVII Neuropathies:
- IDIOPATHIC: Idiopathic Facial Nerve Paralysis
-dogs and cats (cocker spaniels)
-acute, usually unilateral
-reduced tear production
-+/- Ipsilateral peripheral vestibular signs
-localization: peripheral, proximal to geniculate ganglion
-pathology: no inflammation, degeneration of myelinated fibers
-diagnosis of EXCLUSION
-MRI and CSF
-prognosis: good - weeks to months (contracture with chronicity)
-Tx/therapy - eye ointment to prevent exposure keratitis, monitor for KCS/corneal ulcers
-NO corticosteroids - INFECTIOUS: Otitis Media/Interna
- NEOPLASIA:
-Lymphoma
-Compression or invasion of facial nerve caused by tumors of surrounding tissue
(adenomas, adenocarcinomas, squamous cell carcinoma, osteosarcoma, fibrosarcoma etc)
especially of the middle ear and petrous temporal bone
-Brainstem neoplasia may affect the facial nerve (meningioma) - TRAUMA
-bite wounds to head - METABOLIC
-Hypothyroid facial neuropathy in dogs
-Existence is suspected, but NOT proven - INFLAMMATION
-May be associated with polyradiculoneuritis, brachial plexus neuritis - MOTOR UNIT DZ
-myasthenia gravis
Function of the vestibular system? (2)
-maintain steady visual image
-maintain steady body position
Function of the middle ear?
-sound conduction and amplification
-NO vestibular part of middle ear – (no middle ear dz with vestibular dz)
Function of the Inner Ear?
-fxn: balance and equilibrium
-has auditory and vestibular components
-bony labyrinth - perilymph - semicircular canals vestibule
-membranous labyrinth - endolymph - semicircular ducts, utriculus/saaculus
In the vestibular pathway, axons project to: (2)
- vestibular nuclei (in brainstem) - rostral, caudal, medial and lateral; located lateral to the 4th ventricle)
- Vestibular portion of the cerebellum (flocculonodular lobe and fastigial nuclei)
cells of origin - lateral vestibular nucleus
What is peripheral vestibular dz?
-Dz of the receptors or vestibular nerve (issues with the ear – labyrinth or vestibular nerve itself)
nystagmus: horizontal or rotary ONLY (fast phase away from lesion
-non-positional
-conjugate
strabismus: ventral or ventrolateral
-dysconjugate
-ipsilateral to lesion
CNVII deficits are in peripheral OR central vestibular dz – but if more, then it’s CENTRAL dz
associated problems:
-facial nerve/CNVII paresis/paralysis
-Horner’s syndrome
-otitis externa, media-interna
-pain on palpation of bulla/TMJ
-pharyngeal pain
What is central vestibular dz?
Brain issue – dz of the vestibular nuclei (in brainstem), vestibular part of the cerebellum (the floculonodular lobe and the caudal cerebellar penduncles) and pathways
-paradoxical
-nystagmus: can be anything, BUT vertical, positional, dysconjugate ALWAYS central dz ( but CAN BE horizontal/rotary, non-positional, conjugate)
-altered level of consciousness - usually decreased bc of RAS in brainstem
-CN deficits (esp. CNV)
-long tract signs:
–Ascending tracts (sensory). Particularly postural deficits such as loss of conscious
proprioception ipsilateral to the lesion.
–Descending tracts (motor). Paresis or paralysis ipsilateral to the lesion.
-Cerebellar signs
Dysmetria, hypermetria, intention tremor may be present if areas of the cerebellum other than the vestibulocerebellum are involved in the disease process
-seizures
Clinical signs of Vestibular Dz (6)
- Nystagmus (pendular - congenital, or jerk) – named for fast phase (fast phase is away from lesion)
-conjugate or dysconjugate
-horizontal/rotary or vertical (usually central)
-positional or non-positional - Strabismus
- Head tilt (leaning/rolling)
-circling but NO head tilt … not likely vestibular
-tilt towards lesion - Tight circling
-tilt towards lesion - Ataxia
- Nausea +/- vomiting, salivating
vestibular signs are almost always IPSILATERAL to lesion
What is bilateral peripheral vestibular dz?
-No normal or abnormal nystagmus
-Crawling, crouching posture, often falling or staggering to either side
-Characteristic wide head excursions from side to side
-Symmetrical ataxia with preservation of strength
-Flexion of the neck ventrally when suspended by the pelvis
What is central paradoxical vestibular dz?
special form of central vestibular disease, and is termed paradoxical because the vestibular signs are directed to the side OPPOSITE the lesion.
-Head tilt AWAY from the lesion
-Positional ventral strabismus on the side AWAY from the lesion.
-Fast phase of nystagmus TOWARDS the side of the lesion.
need other neurological deficits to recognize
-brainstem signs (CP deficits, paresis, CN deficits) will be ipsilateral to the lesion and will reflect the TRUE laterality of the lesion
Lesions causing paradoxical vestibular disease are usually destructive lesions such as neoplasms or inflammatory disease and often involve the caudal cerebellar peduncle and/or flocculonodular lobe.
Paradoxical signs are probably due to loss of cerebellar inhibition of the vestibular output on the
side of the lesion
When is the auditory system developed in dogs?
Normal hearing developed by 4-5 weeks of age in dogs
What are the types of deafness? (2)
- Peripheral Deafness
a) Conductive deafness: Failure of sound transmission to the inner ear caused by abnormalities
within the external or middle ear cavity
b) Sensorineural deafness: Failure of sound transduction by the spiral organ or failure of
propagation of nerve impulses in the auditory (VIII) nerve - Central
This is RARE. Due to the extensive crossing over of pathways at several levels, lesions causing
central deafness must involve both temporal lobes, or the pathways in the brainstem bilaterally
How is metronidazole related to central vestibular disease?
Doses of metronidazole over 50-60 mg/kg daily have been associated with acute onset of vestibular signs, often with a marked vertical nystagmus and ataxia. Other CNS signs
such as seizures may be apparent
Injury to purkinje cells in cerebellum
What are the 6 lobes of the brain?
- Frontal - behavior, planning, judgement - contains primary motor cortex
- Olfactory - smell – sensory info does NOT go through thalamus
- Parietal - somatosensory - pain, position, temperature, vibrations
- Temporal - auditory
- Occipital - vision
- Limbic - contain hypothalamus, amygdala, etc. - emotion, memory, instinct (4 F’s)
What is MUO?
Meningoencephalitis of unknown origin
MUO describes GME and NME/NLE
GME - granulomatous meningoencephalomyelitis (back of brain dz)
NME/NLE - necrotizing disease
What are the 3 clinical forms of GME (granulomatous meningoencephalomyelitis)?
- ocular
- focal (50% of cases)
- multifocal
brainstem dz is common for GME
Typical signalment of GME?
-typically young breeds
-young to middle-aged
-female>male
Clinical signs of GME?
-vestibular
-long tract signs (postural reaction deficits and paresis)
-cerebellar
-CN deficits
-seizures
MRI and Pathology for GME
-focal vs. multifocal
-variable lesion pattern
-can be normal
-lymphoplasmacytic inflammation
–ENCEPHALITIS and/or MYELITIS
–perivascular cuffing
Typical signalment for NME (Necrotizing Meningoencephalitis)
-small breeds (pug, chihuahua, maltese, pekingnese) - PUG encephalitis
-young (median age 18mo)
-female>male
Pugs can inherit genes for NME – homozygous carriers have 1:8 risk of NME
–genetic test
Clinical Signs of NME (Necrotizing Meningoencephalitis)
- predominantly cerebral
-seizures
-mentation changes
-behavioral changes
-compulsivity, pacing - often asymmetric - circling
seizures is common for NME/NLE
MRI and Pathology for NME
-lymphoplasmacytic inflammation
–MENINGITIS AND ENCEPHALITIS
–necrosis and cavitation
Typical Signalment for Necrotizing Leukoencephalitis (NLE)
-small breeds (yorkie, frenchie, Pomeranian) – YORKIE Encephalitis
-young to middle-aged
-no sex predilection
MRI and Pathology of NLE
-lymphoplasmacytic inflammation
–deep white matter encephalitis
–no meningitis
–necrosis and cavitation
CSF Analysis in Inflammatory Brain Diseases (4)
-pleocytosis (>5 cells)
-elevated protein
-infectious dz testing negative
-can be normal
Definitive diagnosis of Inflammatory Brain Disease
-biopsy
-$$$
Tx for Inflammatory Brain Disease
Immunomodulation
–corticosteroids most widely used
–slowly taper meds once in remission
Adjunctive Immunomodulatory therapies
–to reduce corticosteroid use
–increase treatment efficacy
3 treatment groups:
1. corticosteroids alone
2. corticosteroids + radiation therapy
3. corticosteroids + 1 (or more) adjective drug
Risk factors for Inflammatory Brain Disease
Dz is NOT associated/not risk factors for IBD:
-BCS
-Season
-Time since last vaccination
NO IDEA what the issue is/risk factors are
we know it’s an auto-immune dz, so do we vaccinate or not?
Prognosis for Inflammatory Brain Disease
Postive:
-younger age at diagnostics
-focal dz
-referral within 7 days within onset of signs
Negative:
-seizures, altered mentation
-mass effect, brain herniation on MRI
Outcome:
-33% mortality rate despite tx
-out of remaining 65%, 2/3 will relapse
-survival at one month likely predicts long-term survival
Origin of Primary Brain Tumors
-Neural Tube - astrocytomas, oligodendroglioma
-Neural Crest - meningioma, schwannoma
Meningiomas
-from neural crest
-most common primary tumor in dogs and cats
-median age
-dog: goldens, boxer, min schnauzer
-cat: domestic shorthair
cellular origin: arachnoid vill(?)
extra-axial tumors - surface oriented (outside the brain)
Glioma
-from neural tube
-second most common primary brain tumor in dogs, rare in cats
-astrocytoma FROM astrocytes (supporting cells of CNS)
-oligodendroglioma FROM oligodendrocytes (mylenating cell of the CNS)
-median age
-dog: boxer, boston terrier, bulldog, pitbull
–dogs 50% of gliomas
–boxers 50% of all oligodendroglioma
-intra-axial tumor – from within brain parenchyma
Secondary Brain Tumors (does not originate from brain)
50% of all intracranial neoplasia in dogs
metastatic
-hemangiosarcoma (common in dog)
-lymphoma (younger animals, can be primary) (common in cat)
invasive
-pituitary tumor (common in cat)
Clinical signs with Brain Tumors
CATS
-behavioral changes
-seizures
-altered mentation
-circling
-non-specific lethargy, anorexia
DOGS
-seizures
-circling
-ataxia
-head tilt
-altered mentation
Diagnosis of Brain tumors - what do you need? (4)
- minimum database
- imaging (skull rads, CT, MRI, PET)
- CSF analysis
-intracranial neoplasia = normal cell count + elevated protein
-usually not super helpful - biopsy
What is myoclonus?
a sudden lightning-like involuntary movement of short duration caused by muscle activity
usually focal but can be multifocal
What is a tremor?
Rhythmical oscillatory movement of a body part, mourned an axiom resulting from alternate or synchronous contraction of antagonistic muscle groups
What is an action tremor?
tremor that occurs during voluntary contraction of skeletal muscle
postural and kinetic tremors!
What is a postural tremor?
An action tremor that occurs in a body part that is voluntarily maintained against gravity (eg. standing)
What is a kinetic tremor?
an action tremor that occurs during directed voluntary movement
intention tremor – amplitude increases during pursuit of target
How does Lysosomal Storage Diseases cause tremors?
-rare
-affect CNS - cause tremors
-metabolic by-products accumulate in neurons due to enzyme deficiency
-dz most likely inherited
-young animals <1 year
-many dz affect cerebellum
-genetic testing
-BW and UA
-no effective therapies
-poor prognosis
Cerebellar has 3 cortex layers:
- molecular (superficial)
- purkinje (intermediate)
- granular (deep) – cerebellar nuclei, a lot of neurons
Cerebellar embryology
-from metencephalon
-2 germinal cell migration groups
1. purkinje layer and cerebellar nuclei migrate (don’t divide, just migrate)
2. external germinal layer – goes to surface of cerebellum and divides to 10-12 layers thick, stops diving then migrates into cerebellum, forms the granular cell layer (deep)
late in gestation, post-natal
Clinical signs of cerebellum dysfunction
- ataxia
- dysmetria
- vestibular signs
- menace reaction deficits
- postural reaction deficits
- anisocoria
- increased muscle tone +/- hyperflexia
CS are IPSILATERAL to lesion
