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ACVECC > Neurology > Flashcards

Neurology Flashcards

1
Q

Where is thermoregulatory Center?

A

Preoptic area of the anterior hypothalamus

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2
Q

C1-C5 localization

A
  • 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
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3
Q

C6-T2 localization

A
  • 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
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4
Q

Descending respiratory pathways

A

Automatic
- paramedian reticular formation of medullary & pontine tegmentum
- laterally high cervical spinal cord near spinothalamic tract

Voluntary
- corticospinal tract (brainstem)
- & Upper cervical cord

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5
Q

Hering - Breuer inflation reflex

A

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

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6
Q

Pneumotaxic center

A

Located in Upper pons
- inhibits inspiratory center –> terminates inspiration therefore regulates inspiratory volume and RR

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7
Q

Apneustic Center

A

Located in lower pons
- Sends stimulatory impulses to inspiratory area –> activate and prolong inspiration
** May be over ridden by pneumotaxic center

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8
Q

Medullary respiratory center

A

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

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9
Q

Ascending spinal tracts with nociception

A

Spinothalamic (MC_
Supraspinal
Sipinial reticular

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10
Q

Components of limbic system

A

Cingylate gyrus: behavior/emotion
Locus ceruleus: behavior
Amygdala: fear/anxiety
Hippocampus
Hypothalamus

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11
Q

Generalized tetanus & timeline

A
  • 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
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12
Q

Tetanus immuoglobs

A

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

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13
Q

Tetanus treatment

A
  1. antiserum or hTIG - neutralize circulating
  2. Remove source of infection - wound flush +/- H2O2
    - Abx: clinda, metro, peGm tetracycline
  3. Sedation: benzos +/- barbiturates
    - MgSO4 : supraphysiologic activity
  4. Supportive Care
    - quiet, dark
    - Nutrient support
    - avoid decubital sores
    +/- MV
    +/- indwelling U cath
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14
Q

Localized tetaus

A

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
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15
Q

CN I

A

Olfactory - loss of smell

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16
Q

CN II

A

Optic - loss of vision, absent PLR, or spontaneous fluctuation in pupil size

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17
Q

CN III

A

Oculomotor -abnormal eye movements
- Fixed to direct light and contralateral light
- Normal PLR in contralateral & reacts to light in effected eye
- ventrolateral strabismus & ptosis

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18
Q

CN IV

A

Trochlear - rotary nystagmus

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19
Q

CN V

A

Trigeminal
- Absent PLR & facial sensation
- Masseter & temporal M atrophy
- Enophthalmos (pterygoid m paralysis)

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20
Q

CN VI

A

Abducens
- absent globe retraction ( retraction bulbi muscle paralysis)
- Medial strabismus (lateral rectus m paralysis)

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21
Q

CN VII

A

Facial N
- Lip droop +/- facial droop
- absent menace & palpebral

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22
Q

CN VIII

A

Vestibulocochlear
- head tilt, nystagmus, strabismus, ataxia, walking in tight circles, leaning
- deafness

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23
Q

CN IX

A

Glossopharyngeal
- absent gag reflex

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24
Q

CN X

A

Vagus
- dysphagia

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25
Q

CN XI

A

Spinal accessory
- lar par
- mega esophagus

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26
Q

CN XII

A

Hypoglossal N
-dysphagia
-unilateral tongue atrophy +/- deviation of the tongue

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27
Q

Cheyene stokes breathing

A

Periods of hyperpnea followed by apnea
DDX: diffuse cerebral or thalamic disease
- metabolic encephalopathies

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28
Q

Apneusis

A

Pause in breathing for entire resp cycle
Assd pontine lesions

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29
Q

Central neurologic hyperventilation

A

sustained rapid, fairly deep and regular respirations at 25 bpm with hypocapnia

DDX midbrain, pons lesions

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30
Q

Ataxic breathing

A

irregular breathing in depth and frequency
- precedes complete apnea

** Associated with lower pons & medulla lesions

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31
Q

Reticular formation

A

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
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32
Q

3 respiratory centers

A
  • medulla respiratory center
  • Apneustic center
  • Pneumotaxic Center
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33
Q

Suprapontine Reflex

A

-Interferes with respiration during coughing, sneezing & swallowing

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34
Q

Central Chemo receptors

A
  • Ventral surface of medulla (increased PaCO2 –> increased CSF H+ –> crosses BBB –> changed ventilation)
  • Respiration for 85% respiratory response to CO2
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35
Q

DAMNIT-V

A

Degenerative - IVDD
Anomalies: congent malform
Metabolic: sock, DM, hypoBG, Na changes)
Neoplasia
Infect, Inflamm, Idiopathic
Toxin, Trauma
Vascular

36
Q

Contraindications to CSF sampling

A
  1. Anesthesia that increases ICP
  2. Acute TBI
  3. Coagulopathies
  4. Severe &/or rapidly progressing increased ICP
  5. A-A lux or craiocervical Fx or lux

RISKS: traumato cerebellum, brainstem or cervical cord, vestibular syndrome (self limiting), or apnea (poss life threatening)

37
Q

Indications for CSF sampling

A

CNS Signs consistent with primary CNS disease:

  1. Susp infectious/inflamm disease affecting CNS
  2. Susp neoplastic Dz affecting CNS
  3. Cluster or continuous seizures
  4. Acute ascending LMN signs
38
Q

States of consciousness

A
  1. Normal: for that animal
  2. Obtunded: decreased responsiveness (may be mild, moderate or severe)
  3. Stuporous: responds only to vigorous painful stimuli
  4. Coma: does not respond
39
Q

Types of Acquired myasthenia Gravis

A

** 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

40
Q

Peripheral chemoreceptors

A
  1. 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
  2. Aortic bodies: regulate circulation
41
Q

Nerve fibers for inspiration

A
  • Ventral horns C3-C5 –> phrenic motor
  • Ventral horns T2-T12–> external intercostal motor
42
Q

Spinal shock

A

If examined soon after injury
- decreased segmental reflexes caudal to injury despite arcs being intact
- May last 12-24 hours

43
Q

Hepatocutaneous Syndrome

A

Hyperkeratosis & crusting/fissuring of paw pads
- erythema, erosions, and hyperkeratosis of perioral, perivulvar, preputial and scrotal skin

44
Q

Neurologic scoring system myelopathy

A

Grade 1: no deficits
Grade 2: paresis; walking
Grade 3: paresis nonambulatory
Grade 4: paralysis
Grade 5: paralysis, no deep pain

45
Q

Cerebral autoregulation

A
  • Only present BTW cerebral perfusion pressure of 50-150 mmHg
  • Changes in transmural tone result in changes in cerebrovascular tone
46
Q

Chemical Autoregulation of cerebral vascular resistance

A
  1. PaCO2: Co2 + H2O –> H+ which when go up cause vasodilation & when goes down may cause vasoconstriction
  2. PaO2: decreased PaO2 causes vasodilation –> increased CBF, CBV, & ICP
  3. Cerebral metabolic rate of O2 consumption: areas of increased metabolic activity result in increased H+ –> increased cerebral blood flow
47
Q

Loss corneal N reflexes

A
  • Corneal touch –> bilateral eye closure
  • If Absent:
    afferent trigeminal (CN V) & efferent Facial (CN VII) OR relex connection in pons & medulla
48
Q

Resting eye position

A

Medial rectus paresis: CN III damage

Lateral Rectus Paresis: CN VI damage, rostral oblongata or pons

** important for TBI

49
Q

Oculovestibular movements

A

Midbrain & pons

= Nuclei of CN III, IV & VI

50
Q

mastecatory myositis

A
  • 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

51
Q

Trigeminal neuritis

A
  • 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

52
Q

Myasthenia Dx & Tx

A

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

53
Q

LMN Dz

A
  1. Myasthenia
  2. Botulism
  3. Tick paralysis
  4. Elapid Envenomation
  5. Coonhound paralysis (polyradiculitis)

**Aminoglycosides can trigger/worsen LMN disease in animals (reversible)

54
Q

Botulism

A
  • 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

55
Q

Metabolic disease to cause altered mentation

A
  • 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
56
Q

Drugs that may alter mentation

A
  • Anticonvulsents
  • Benzos
  • opiates
  • anesthetics
  • atropine
  • steroids
  • Abx (pens, cephs, fluoros, aminos, metro)
  • H2R blockers
  • Cardiac glycosides
  • antihypertensives
  • illicits
57
Q

Oculocephalic reflex

A
  • 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

58
Q

Sites for CSF tap

A

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

59
Q

ICP: what it measures; locations to measure

A

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

60
Q

+/- of different transducers for ICP monitoring

A

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

61
Q

“Normal” ICP

A
  • 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

62
Q

Indications for ICP monitoring

A
  1. Anesthetized or comatose animals undergoing/recovering from intracranial surgery
  2. Severe progressive neuro deterioration associated with disease such as infect/inflammm
  3. Severe, traumatic head injury
  4. research animals
63
Q

Forebrain lesions (neuro exam findings)

A

-Abnormal consciousness
- +/- decerebrate rigidity head turn
- Wide circling or CP deficits
- Seizures
+/- CN deficits

64
Q

Cerebellum lesions (neuro exam findings)

A
  • Normal Mentation
  • Decerebellate rigidity
  • Tight circling
  • CP deficits
  • hypermetria
  • intention tremors
  • absent menace
  • Anisocoria
65
Q

Brainstem lesions (neuro exam findings)

A
  • Abnormal consciousness
  • Decerebrate rigidity
  • CP deficits
  • No changes in movement
    +/- CN changes
66
Q

Decerebellate posture

A
  • Rigid extention of forelimbs
  • relaxed pelvic limbs in any posture
  • mentation normal

**Cerebellar injury

67
Q

Decerebrate rigidity

A
  • Rigid extension of thoracic and pelvic and neck
  • Mentation typically abnormal

**Brainstem disease or forebrain

Poor prognosis

68
Q

Peripheral nerve localization

A
  • paresis/paralysis
  • CP deficits
  • Reflex deficits
69
Q

NMJ localization

A
  • Paresis/paralysis
  • CP deficits
  • Reflex deficits
  • Stiff, stilted gait
70
Q

Muscle localization

A
  • paresis/paralysis
  • stiff stilted gait
  • normals CPs & reflexes
71
Q

Spinal cord segments & vertebral bodies

A
  • 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
72
Q

SChiff Scherrington posture

A
  • 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

73
Q

L4- S3 myelopathy

A

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

74
Q

T3-L3 myelopathy

A

Thoracic: normal reflexes, normal CPs

Pelvic: normal reflexes, decreased CPS
- Ataxia, short stride length due to dysfunction of ascending proprioceptive tracts

*Schiff scherrington

75
Q

LMN vs UMN

A

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

76
Q

Peripheral vestibular exam findings

A
  • 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
77
Q

Central vestibular exam findings

A
  • 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
78
Q

Paradoxical head tilt

A
  • opposite to lesion
  • seen if lesion cerebellar
79
Q

Horners Syndrome

A
  • miosis
  • ptosis
  • enophthalmos
  • protrusion of 3rd eyelid

**Middle or oinner ear disease –> in tympanic bulla - vagosympathetic trunk

80
Q

Toxic vestibular etiologies

A

Peripheral:
- aminoglycosides
- furosemide
- chlorohexidine
- 10% fiprinil sol.

Central:
- metronidazole
- lead

81
Q

Etiologies of Peripheral vestibular disease

A
  • congenital vestibular disease
  • hypothyroid
  • idiopathic
  • trauma from ear flush or bulla osteotomy
  • neoplasia
82
Q

Etiologies of central vestibular disease

A
  • degenerative–> cerebellar lysosomal storage disease
  • hydrocephalous
  • intra-arachnoid cyst
  • Hypothyroid
  • thiamine deficiency
  • head trauma
  • vascular disease
  • neoplasia
83
Q

INfectious causes of central vestibular disease

A
  • 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)
84
Q

Admission BP and HR and sens/spc for brain herniation

A

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)

85
Q

Guidelines for therapy of Intracranial hypertension

A
  1. Maintain CPP: ideally btw 50-90 mmHg
    - MAP at >80 if unable to monitor ICP (and therefore CPP)
  2. Decreased cerebral venous volume
    - elevate head
    - Avoid: neck wraps, improper positioning of head/neck & PEEP
  3. Control PaCO2 most important factor
    - Target PaCO2 30-35 mmHg (lower values may lead to neural ischemia – exacerbate ICH)
    - Controlled vent for vasoconstriction
  4. Control PaO2
    - Target normal –> sig increase in CBF at PaO2 <60 mmHg
  5. Reduce cerebral edema –> hyperosmolar therapy
86
Q

PArts of neuro exam

A
  1. Mentation/general opbservations
  2. Gait/posture
  3. CN exam
  4. Segmental reflexes
  5. Proprioceptive placing
  6. +/- pain sensation/nociception

ACVECC (10 decks)

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