Neurology Flashcards
Where is thermoregulatory Center?
Preoptic area of the anterior hypothalamus
C1-C5 localization
- Normal mentation & posture
- Thoracic: CP deficits, normal to inc. reflexes
- Pelvic: CP deficits, normal to inc reflexes
- Long strided or ‘floating’ thoracic & pelvic limb gait
+/- shallow respiration –> phrenic N & intercostal N
C6-T2 localization
- Thoracic: CP deficits, decreased reflexes (LMN)
- Pelvic: CP deficits, normal to inc reflex (UMN)
- Two engine gait: short stride front, ataxia hind
- Horner’s syndrome from damage of the sympathetic fibers at this level
Descending respiratory pathways
Automatic
- paramedian reticular formation of medullary & pontine tegmentum
- laterally high cervical spinal cord near spinothalamic tract
Voluntary
- corticospinal tract (brainstem)
- & Upper cervical cord
Hering - Breuer inflation reflex
Excessive stretching of pulmonary stretch receptors –> send impulses through myelinated fibers of vagus to insp area medulla & apneustic –> inhibit insp discharge –> decreased RR by increased expiratory time
Pneumotaxic center
Located in Upper pons
- inhibits inspiratory center –> terminates inspiration therefore regulates inspiratory volume and RR
Apneustic Center
Located in lower pons
- Sends stimulatory impulses to inspiratory area –> activate and prolong inspiration
** May be over ridden by pneumotaxic center
Medullary respiratory center
2 sites: ventral & Dorsal
Dorsal ( nucleus solitarus CN IX & X)
- inspiratory rhythm
Ventral
- forced inhalation ad exhalation
- 4 nuclei: N. retroambiguus, N paraambiguus, N. retrafacialis, pre-botziger complex
Ascending spinal tracts with nociception
Spinothalamic (MC_
Supraspinal
Sipinial reticular
Components of limbic system
Cingylate gyrus: behavior/emotion
Locus ceruleus: behavior
Amygdala: fear/anxiety
Hippocampus
Hypothalamus
Generalized tetanus & timeline
- CS in 5-12 days up to 4 weeks after onset of infection
- Extreme muscle rigidity –> extensor groups mostly effected
- outstretched tail, hypertonic myotactic reflexes & normal CPs
- CN involvement vary, risus sardonicus, trismus (lock jaw), protrusion 3rd eyelids, enophthalmus, laryngeal spasm, dysphagia
- 3 week recovery since have to make new nerve terminals
Tetanus immuoglobs
Equine ATS -antitetaus serum –> IV & IM
hTIG - tetanus immuoglob –> IM only
** Only work if toxin in blood –> cannot cross BBB
Dose based on toxin load
Reactions:
1. Anaphylactitc –> IgE (type I hypersensitivity)
2. Anaphylactoid –> mast cell degranulation
3. Serum sickness –> type III hypersensitivity
Tetanus treatment
- antiserum or hTIG - neutralize circulating
- Remove source of infection - wound flush +/- H2O2
- Abx: clinda, metro, peGm tetracycline - Sedation: benzos +/- barbiturates
- MgSO4 : supraphysiologic activity - Supportive Care
- quiet, dark
- Nutrient support
- avoid decubital sores
+/- MV
+/- indwelling U cath
Localized tetaus
Lower toxin load
- muscle rigidity only at site of infection –> may progress to generalized
- Controlateral limb 2nd to be effects
- C involvement late in infection
CN I
Olfactory - loss of smell
CN II
Optic - loss of vision, absent PLR, or spontaneous fluctuation in pupil size
CN III
Oculomotor -abnormal eye movements
- Fixed to direct light and contralateral light
- Normal PLR in contralateral & reacts to light in effected eye
- ventrolateral strabismus & ptosis
CN IV
Trochlear - rotary nystagmus
CN V
Trigeminal
- Absent PLR & facial sensation
- Masseter & temporal M atrophy
- Enophthalmos (pterygoid m paralysis)
CN VI
Abducens
- absent globe retraction ( retraction bulbi muscle paralysis)
- Medial strabismus (lateral rectus m paralysis)
CN VII
Facial N
- Lip droop +/- facial droop
- absent menace & palpebral
CN VIII
Vestibulocochlear
- head tilt, nystagmus, strabismus, ataxia, walking in tight circles, leaning
- deafness
CN IX
Glossopharyngeal
- absent gag reflex
CN X
Vagus
- dysphagia
CN XI
Spinal accessory
- lar par
- mega esophagus
CN XII
Hypoglossal N
-dysphagia
-unilateral tongue atrophy +/- deviation of the tongue
Cheyene stokes breathing
Periods of hyperpnea followed by apnea
DDX: diffuse cerebral or thalamic disease
- metabolic encephalopathies
Apneusis
Pause in breathing for entire resp cycle
Assd pontine lesions
Central neurologic hyperventilation
sustained rapid, fairly deep and regular respirations at 25 bpm with hypocapnia
DDX midbrain, pons lesions
Ataxic breathing
irregular breathing in depth and frequency
- precedes complete apnea
** Associated with lower pons & medulla lesions
Reticular formation
AKA ascending RAS
-Network of nuclei in brainstem that act to activate cerebral cortex & maintain consciousness
- Midbrain, rostral pons, & thalamus–> most important for maintaining consciousess
3 respiratory centers
- medulla respiratory center
- Apneustic center
- Pneumotaxic Center
Suprapontine Reflex
-Interferes with respiration during coughing, sneezing & swallowing
Central Chemo receptors
- Ventral surface of medulla (increased PaCO2 –> increased CSF H+ –> crosses BBB –> changed ventilation)
- Respiration for 85% respiratory response to CO2
DAMNIT-V
Degenerative - IVDD
Anomalies: congent malform
Metabolic: sock, DM, hypoBG, Na changes)
Neoplasia
Infect, Inflamm, Idiopathic
Toxin, Trauma
Vascular
Contraindications to CSF sampling
- Anesthesia that increases ICP
- Acute TBI
- Coagulopathies
- Severe &/or rapidly progressing increased ICP
- A-A lux or craiocervical Fx or lux
RISKS: traumato cerebellum, brainstem or cervical cord, vestibular syndrome (self limiting), or apnea (poss life threatening)
Indications for CSF sampling
CNS Signs consistent with primary CNS disease:
- Susp infectious/inflamm disease affecting CNS
- Susp neoplastic Dz affecting CNS
- Cluster or continuous seizures
- Acute ascending LMN signs
States of consciousness
- Normal: for that animal
- Obtunded: decreased responsiveness (may be mild, moderate or severe)
- Stuporous: responds only to vigorous painful stimuli
- Coma: does not respond
Types of Acquired myasthenia Gravis
** Antibodies against Ach receptors
Focal MG: pharyngeal or laryngeal dysfunction without appendicular muscle involvement
- Ptyalism, dysphagia, dysphonia, retching, MegaE
Generalized MG: appendicular m weakness
- strength returns after periods of rest
- Stiff, short strided gait, ** CPs and REFLEXES normal!!!
Treatment: pyridostigmine
Acute Fulminant: severe, sudden appendicular weakness resulting in recumbency, laryngeal dysfunction
Peripheral chemoreceptors
- Carotid bodies:
- decreased PO2 –> increased ventilation
- Decreased pH –> increased ventilation regardless of cause
**Decreased sensitivity to ventilation than aortic
** Less degree of effect on vent compared to central chemoreceptors but act more quickly - Aortic bodies: regulate circulation
Nerve fibers for inspiration
- Ventral horns C3-C5 –> phrenic motor
- Ventral horns T2-T12–> external intercostal motor
Spinal shock
If examined soon after injury
- decreased segmental reflexes caudal to injury despite arcs being intact
- May last 12-24 hours
Hepatocutaneous Syndrome
Hyperkeratosis & crusting/fissuring of paw pads
- erythema, erosions, and hyperkeratosis of perioral, perivulvar, preputial and scrotal skin
Neurologic scoring system myelopathy
Grade 1: no deficits
Grade 2: paresis; walking
Grade 3: paresis nonambulatory
Grade 4: paralysis
Grade 5: paralysis, no deep pain
Cerebral autoregulation
- Only present BTW cerebral perfusion pressure of 50-150 mmHg
- Changes in transmural tone result in changes in cerebrovascular tone
Chemical Autoregulation of cerebral vascular resistance
- PaCO2: Co2 + H2O –> H+ which when go up cause vasodilation & when goes down may cause vasoconstriction
- PaO2: decreased PaO2 causes vasodilation –> increased CBF, CBV, & ICP
- Cerebral metabolic rate of O2 consumption: areas of increased metabolic activity result in increased H+ –> increased cerebral blood flow
Loss corneal N reflexes
- Corneal touch –> bilateral eye closure
- If Absent:
afferent trigeminal (CN V) & efferent Facial (CN VII) OR relex connection in pons & medulla
Resting eye position
Medial rectus paresis: CN III damage
Lateral Rectus Paresis: CN VI damage, rostral oblongata or pons
** important for TBI
Oculovestibular movements
Midbrain & pons
= Nuclei of CN III, IV & VI
mastecatory myositis
- Swelling & pain of temporaliss, masseter, & pterygoid muscles
- If untreated may progress to atrophy of masticatory m and difficulty prehending food
- Confirmed with muscle biopsy or serum aby against type IIM muscle fiber
Tx: immunosuppressives
Trigeminal neuritis
- Bilateral mandibular muscle paralysis +/- decreased facial sensation or hyperesthesia
- Acutely unable to close mouth, difficulty e/d & severe ptyalism
+/- horners if inflammation gets to ophth. branch
- Tx: supportive care, meatball food, elevate head, tape muzzle
** Recover 2-4 weeks
DDX: rabies, round cell tumor, polyneuritis
Myasthenia Dx & Tx
DX:
- aby detected 80-90% dogs with acquired disease
- Intercostal muscle bx –> ID aby @ NMJ
- Edrophonium test: dramatic improvement in gait up to 2 min after injection (unless fulminant in form)–> pretreat with atropine to avoid SLUDD
TX:
- plasmapharesis, IVIG, pytridostigmine
- Acquired MG may resolve
- Acute fulminant often fatal
LMN Dz
- Myasthenia
- Botulism
- Tick paralysis
- Elapid Envenomation
- Coonhound paralysis (polyradiculitis)
**Aminoglycosides can trigger/worsen LMN disease in animals (reversible)
Botulism
- Clostridium botulinum
- Hours-days post ingestion
- interferes with release of Ach from NMJ
CS: flaccid tetraplegia, decreased reflexes, CN affected, +/- autonomic signs (urine retention, mydriasis, decreased tear production, constipation)
TX: supportive care 2-3 weeks; type C antitoxin early in disease
Metabolic disease to cause altered mentation
- Hypoxia (anemia, methemoglob, pulm dz)
- Ischemia
- hypoglycemia
- HE/uremic enceph
- Endocrine dysfunction (thyroid, adrenal, pancreas)
- Pit apoplexy
- Sepsis
- Kernicterus (inc bilirubin)
- hyper/hypothermia
- pain
- post ictal
- acidosis/alkalosis
- electrolyte abnormalities
Drugs that may alter mentation
- Anticonvulsents
- Benzos
- opiates
- anesthetics
- atropine
- steroids
- Abx (pens, cephs, fluoros, aminos, metro)
- H2R blockers
- Cardiac glycosides
- antihypertensives
- illicits
Oculocephalic reflex
- physiologic nystagmus
- Loss assd with lesions of medial longitudinal fasiculus in Pons & medulla –» coord function of CN III, IV, & VI
**Indicates poor prognosis if lost
Sites for CSF tap
Cranial: palpate occipital protuberance, spinous process of C2, dorsal arch C1 & wings of atlas
- Center of triangle of wings & occiput
Lumbar
- Lrg breed: L4-5
- Small breed: L5-6
- Cats L6-7
ICP: what it measures; locations to measure
Total ICP 3 components:
- Hydrostatic P influenced by gravity
- atmospheric P: inc altitude = increased ICP
- Filling P: volume of fluid in cranial vault
Sites:
Subdural/epidural options
- lateral ventricles/subarachnoid space
-intraparenchymal
+/- of different transducers for ICP monitoring
External P transducer:
- Pro: accurate, calibrated after insertion, min zero drift, less expensive
-Con: may obstruct & give false reads, measure at fixed ref points, little patient movement, leakage
Internal P Transducer
- Pro: accurate, easy to place, patient can move
- Con: no zero post insertion, zero drift, increased cost
“Normal” ICP
- for dog & cat varies between 5-12 mmHg
-Wave form similar to arterial wave affected by cardiac & Resp changes
**Treatment recommended at 15-20 mmHg
Indications for ICP monitoring
- Anesthetized or comatose animals undergoing/recovering from intracranial surgery
- Severe progressive neuro deterioration associated with disease such as infect/inflammm
- Severe, traumatic head injury
- research animals
Forebrain lesions (neuro exam findings)
-Abnormal consciousness
- +/- decerebrate rigidity head turn
- Wide circling or CP deficits
- Seizures
+/- CN deficits
Cerebellum lesions (neuro exam findings)
- Normal Mentation
- Decerebellate rigidity
- Tight circling
- CP deficits
- hypermetria
- intention tremors
- absent menace
- Anisocoria
Brainstem lesions (neuro exam findings)
- Abnormal consciousness
- Decerebrate rigidity
- CP deficits
- No changes in movement
+/- CN changes
Decerebellate posture
- Rigid extention of forelimbs
- relaxed pelvic limbs in any posture
- mentation normal
**Cerebellar injury
Decerebrate rigidity
- Rigid extension of thoracic and pelvic and neck
- Mentation typically abnormal
**Brainstem disease or forebrain
Poor prognosis
Peripheral nerve localization
- paresis/paralysis
- CP deficits
- Reflex deficits
NMJ localization
- Paresis/paralysis
- CP deficits
- Reflex deficits
- Stiff, stilted gait
Muscle localization
- paresis/paralysis
- stiff stilted gait
- normals CPs & reflexes
Spinal cord segments & vertebral bodies
- C1, C2, T13, L1 & L2 are only SC segments that are in corresponding vertebral bodies
- Caudal spine: SC segment lies in vertebrae CRANIAL to vertebrae with same number
- SC segment L7, S1-3 & Cd1 may be present in L5 vertebral body
SChiff Scherrington posture
- Rigid extension forelimbs and neck
- variable pelvic limbs
-laterally recumbent - T3-L3 myelopathy
**Not assd with worse prognosis
*Due to lack of inhibitory ascending input to thoracic limbs originating from border cells in lower thoracic & lumbar spinal cord
L4- S3 myelopathy
Thoracic: normal reflexes & CPs
Pelvic: decreased reflexes & CPs
- more caudal lesion –> more LMN signs
L4-S1: lumbar intumescence & give rise to femoral, obturator, sciatic, pelvic and pudendal
S1-S3: short strided with shuffle paws
T3-L3 myelopathy
Thoracic: normal reflexes, normal CPs
Pelvic: normal reflexes, decreased CPS
- Ataxia, short stride length due to dysfunction of ascending proprioceptive tracts
*Schiff scherrington
LMN vs UMN
LMN signs: flaccid, decreased segmental reflexes, rapid muscle atrophy (1-2wks), absent/decreased CPs
UMN signs: increased tone, increased segmental reflexes, spastic paresis/paralysis, absent/dec CPs
Peripheral vestibular exam findings
- Normal consciousness
- head tilt toward lesion
- Ataxia
- Nomovement changes/disoiented
- CN VII deficits ipsilateral
- Nystagmus–> fast phase away from lesion, rarely positional
- Strabismus
- Horners common ipsilateral
- infrequent circling
Central vestibular exam findings
- Abnormal consciousness
- head tilt ipsilateral or contralateral
- Ataxia
- hypermetria
- CN V, VII, IX, X, XII deficits ipsilateral
- Nystagmus (any variety)
- Strabismus
- head tremors if cerebellar
- Circling toward lesion
- Decreased CPs ipsilateral
Paradoxical head tilt
- opposite to lesion
- seen if lesion cerebellar
Horners Syndrome
- miosis
- ptosis
- enophthalmos
- protrusion of 3rd eyelid
**Middle or oinner ear disease –> in tympanic bulla - vagosympathetic trunk
Toxic vestibular etiologies
Peripheral:
- aminoglycosides
- furosemide
- chlorohexidine
- 10% fiprinil sol.
Central:
- metronidazole
- lead
Etiologies of Peripheral vestibular disease
- congenital vestibular disease
- hypothyroid
- idiopathic
- trauma from ear flush or bulla osteotomy
- neoplasia
Etiologies of central vestibular disease
- degenerative–> cerebellar lysosomal storage disease
- hydrocephalous
- intra-arachnoid cyst
- Hypothyroid
- thiamine deficiency
- head trauma
- vascular disease
- neoplasia
INfectious causes of central vestibular disease
- Viral: FIP, FIV, FeLV, rabies, pseudorabies, borna disease virus, distemper
- Protozoa: toxoplasmosis, neospora, encephalitozoonosis
- Bacterial aerobes & anaerobes
- Rickettsia rickettsii & erlichia species
- Fungal: crypto, blasto, histo, coccidiosis, aspergillus
- Parasites: HW, cuterebra, angiostrongylus
- Unknown agents: nonsupp meningoencephalitis, necrotizing meningoencephalitis (terries, pugs, maltese), or necrotizing leukoencephalitis (yorkies)
Admission BP and HR and sens/spc for brain herniation
A combination of an SBP > 140 mm Hg and HR < 80/min provided 24% sensitivity and 100% specificity to diagnose dogs with brain herniation (P < 0.0001)
Guidelines for therapy of Intracranial hypertension
- Maintain CPP: ideally btw 50-90 mmHg
- MAP at >80 if unable to monitor ICP (and therefore CPP) - Decreased cerebral venous volume
- elevate head
- Avoid: neck wraps, improper positioning of head/neck & PEEP - Control PaCO2 most important factor
- Target PaCO2 30-35 mmHg (lower values may lead to neural ischemia – exacerbate ICH)
- Controlled vent for vasoconstriction - Control PaO2
- Target normal –> sig increase in CBF at PaO2 <60 mmHg - Reduce cerebral edema –> hyperosmolar therapy
PArts of neuro exam
- Mentation/general opbservations
- Gait/posture
- CN exam
- Segmental reflexes
- Proprioceptive placing
- +/- pain sensation/nociception
