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Dog & Cat Medicine and Surgery > James - Neurology > Flashcards

James - Neurology Flashcards

1
Q

VITAMINN D - what do the letters stand for?

A
  • Vascular accidents
  • Immune-­‐mediated / infecTous encephaliTs
  • Trauma
  • Anomaly: congenital malformaTon (parenchyma, meninges) • Metabolic: hepaTc, renal encephalopathies
  • Idiopathic: geneTc (idiopathic) epilepsy
  • Neoplasia: brain tumours
  • NutriTon: thiamine deficiency
  • DegeneraTve: storage diseases
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2
Q

What can cause encephalitis (inflammation of the brain)?

Infectious(6)/non-infectious

A
  1. Inflammatory/infectious
    a) Viral: CDV, FIP, rabies
    b) Rickettsial (very tiny gram -ve, obligate intracellular bacteria): Ehrlichia canis, RMS
    c) Bacterial(3): Staph, strep, coliforms
    d) Fungal(5): blastomycosis, Histoplasmosis, cryptococcus, coccidioides, aspergillosis
    e) Protozoal: Toxoplasma, neospora
    f) Parasititc: verminous, larval migrans, cysticercosis
  2. Non-infectious (immune-mediated) - approx 99% in Ontario
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3
Q

What structures are affected with GME? (Granulomatous meningoencephilitis)

A

Brain, spinal cord, meninges, can be optical (CN II)

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4
Q

What is the breed disposition for necrotizing encephalitis?

A

Small breeds, younger age (2-5 y)
e.g. pugs, maltese, chihuahua for NME
yorkshire terriers for NLE (Necrotizing Leukoencephalitis)

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5
Q

What is the difference between NME and NLE

A

Necrotizing meningoencephalitis
Necrotizing Leukoencephalitis

NME - immune-mediated against astrocytes, cerebrum/leptomeninges involved.
NLE - brainstem commonly involved (sometimes the cerebrum/leptomeninges)
Both affect grey & white matter

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6
Q

What is Necrotizing encephalitis?

A

NME - Cerebral & white matter + meningitis
NLE - Brainstem, cerebral white matter
–> eating away from mild edema

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7
Q

Necrotizing encephalitis - Diagnostic tests

A 
CBC/profile/UA
Thoracic rads, abdominal ultrasound
MRI (brain +/- spinal cord
CSF analysis -> inc. nucleated cells/inc TP
Titres, PCRs
HIstopathology (definative)
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8
Q

Necrotizing encephalitis - Diagnostic tests for infectious cause suspected

A

Titres, PCRs

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9
Q

Brain tumours - signalment

A

Older dogs & cats

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10
Q

Brain tumours - primary (5)? Secondary (2)?

A

Primary(5): neurons, glial cells(supportive, form myelin), choroid plexus, ependymal (thin membrane lining the ventricles), meninges
Secondary: local extension, metastases

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11
Q

Most common primary brain tumour? Other common ones?

A

Meningoma
Glioma (astrocytoma, oligodendroglioma, glioblastoma)
Choroid plesus tumour (papilloma vs. carcinoma)
Ependymoma

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12
Q

Secondary Brain tumours - local extension (4)

A 
Local extension:
•  Calvarial (osteosarcoma, MLO) 
•  Nasal carcinoma
•  Pituitary tumour
•  PNST (CN V)
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13
Q

Secondary Brain tumours - metastatic (4)

A 
Metastatic: 
•  HSA (hemangiosarcoma)
•  LSA (lymphosarcoma)
•  Carcinoma – mammary, pulmonary, prostatic
•  Malignant melanoma
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14
Q

Brain Tumours Treatment
Factors for choice
4 options with details

A
  • Factors: tumour type, location, morbidity/mortality, cost
  • Corticosteroids
  • Chemotherapy: lomustine, hydroxyurea, cytosine arabinoside
  • Radiation therapy: linear accelerator, gamma knife
  • Surgery
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15
Q

Metabolic Encephalopathies - what parts of the body cause these?

A

Cerebrocortical neurones are most susceptible to metabolic disrutpion (high energy demands, litter reserve)
Hepatic encepalopathy (congenital PSS, microvascular dysplasia, acutehepatotoxicity)
Renal encephalopathy (aka uremic encephalopathy)
Others:
Hypoglycemia
Electrolyte imbalances (e.g. sodium)
Hypoperfusion

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16
Q

Metabolic Encephalopathies - clinical signs

A 
Clinical Signs:
•  Symmetrical (whole system affected)
•  ThalamocorTcal
•  Depression, disorientaTon •  Pacing, head pressing
•  Menace response deficits •  Seizures
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17
Q

Examples of congenital disorders

A

• Hydrocephalus
ly means a smooth brain without evidence
eopallium.
rtical fo•l diAngratochpnrooduidcecgysritsa,ndlysuslcei.nIct eispahaly, etc.

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18
Q

Circling to the right?

A

Thalamo-cortex, right (Direction they circle in is not contra)

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19
Q

Neurological exam

A
  • MentaTon
  • Gait & Posture
  • Cranial Nerves
  • Postural ReacTons
  • Spinal Reflexes
  • PalpaTon (Spinal Pain)
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20
Q

Depressed/obtunded - what is it & where is the lesion?

A
  • Drowsiness, inattention, less responsive to environment
  • Brainstem (ARAS)
  • Thalamocortex
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21
Q

Stuporous - what is it & where is the lesion

A
  • Unconsciousness +êresponsiveness • Can be aroused with noxious sTmulus • ParTal disconnecTon
  • Brainstem (ARAS)
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22
Q

Comatose - what is it & where is the lesion

A
  • Unconsciousness + NO responsiveness • Total disconnecTon
  • Reflexes may be intact
  • Brainstem (ARAS)
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23
Q

Disoriented - where is the lesion

A

• Thalamocortex &/or vestibulocerebellar

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24
Q

Thalamocortex: NE

A
  • Mentation: depression / delirium / disorientation / Δ behaviour
  • Head pressing, compulsion, wandering, pacing
  • Gait & Posture: circling (ipsi), body turn (ipsi pleurothotonus)
  • Mild hemiparesis (contra)
  • Cranial Nerves: menace & nasal septum responses (contra)
  • Postural Reactions (contra, almost normal gait)
  • Spinal Reflexes
  • PalpaTon (Spinal Pain): possible neck pain
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25
Q

Cranial Nerves: Tests

A
  • Menace response (II, VII, cortex, cerebellum) • PLRs (II, III)
  • Physiological nystagmus (VIII, MLF, III, IV, VI) • Nasal septum response (Vs, cortex)
  • Muscles of masTcaTon (Vm) • Palpebral reflexes (Vs, VII)
  • Facial symmetry (VII)
  • Head Tlt (VIII)
  • Swallow (IX, X, XII) • Voice (X)
  • Tongue tone (XII)
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26
Q

Brainstem: NE

A
  • Mentation: depression / stupor / coma
  • Gait & Posture:
    * UMN tetra/hemiparesis/plegia
    * Decerebrate rigidity / opisthotonus
    * Vestibular ataxia
  • Cranial Nerves:
    * Deficits III -­‐ XII
  • Postural ReacTons:
    * Deficits all limbs (ipsi)
  • Spinal Reflexes: NAF
  • PalpaTon (Spinal Pain): possible neck pain
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27
Q

Encephalopathy: Clinical Signs

A
  • Thalamocortex ± Brainstem ± Cerebellum
  • Lesion localizaTon: diffuse vs mulTfocal
  • Beware the focal lesion:
  • Extensive mass invading mulTple CNS regions
  • Focal lesion w/ extensive 2nd surrounding edema • Focal obstrucTon of CSF flowèhydrocephalus
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28
Q

EncephaliTs: Differentials

A
  • Vascular accidents
  • Immune-­‐mediated / infecTous encephaliTs
  • Trauma
  • Anomaly: congenital malformaTon (parenchyma, meninges) • Metabolic: hepaTc, renal encephalopathies
  • Idiopathic: geneTc (idiopathic) epilepsy
  • Neoplasia: brain tumours
  • NutriTon: thiamine deficiency
  • DegeneraTve: storage diseases
29
Q

EncephaliTs: Clinical Signs

A

MulTfocal / diffuse CNS • Acute / subacute

• Progressive

30
Q

What areas are there problems in for the following:
encephalitis
Brain
MyeliTs

A

Spinal Cord
Meningitis
Meninges

31
Q

Infectious Encephalitis

A
  • Viral: CDV, FIP, rabies…
  • RickeOsial: Ehrlichia canis, RMS
  • Bacterial: Staph, Strep, coliforms
  • Fungal: blasto, histo, crypto, coccidioides, aspergillosis • Protozoal: Toxoplasma, Neospora
  • ParasiTc: verminous, larval migrans, cysTcercosis…
32
Q

What is a seizure?

A

Seizure: A transient occurrence of signs due to abnormal excessive or synchronous neuronal acRvity in the thalamus & cerebral cortex (thalamocortex)
NeurolocalizaRon: Thalamocortex

33
Q

What is epilepsy?

A

Epilepsy: A condiRon of recurrent seizures due to a chronic brain disorder

34
Q

Prodrome:

A

Period preceding seizure, consisRng of a change in sensorium of paRent exhibited in behaviour; ~ hrs – days

35
Q

Aura:

A

IniRal motor or sensory signs of a seizure; ~ seconds

36
Q

Ictus:

A

Seizure itself

37
Q

Post-­‐ictus:

A

Recovery period with transient abnormaliRes, e.g. mentaRon, menace, gait; ~ minutes – days

38
Q

Timing of seizures

A

Singles (self-limited) - Isolated
Cluster - >= 2 in 24, recover in between
Status Epilepticus - continuous

39
Q

Generalized Seizure (previously Grand mal)

A
  • Originates at some point within & rapidly engaging bilateral networks
  • LocaRon & lateralizaRon not necessarily consistent
  • Usually symmetric (may be asymmetric)
  • Consciousness oben impaired
  • Previously known as “grand mal”
40
Q

Focal Seizures

A
  • Originate w/in networks limited to 1 hemisphere (unilateral)
  • Ictal onset consistent between seizures
  • PreferenRal propagaRon paeerns may include other hemisphere (“secondarily generalized”)
  • ± Impairment of consciousness
  • Previously known as:
    * Petit mal
    * Partial
    * Simple partial
    * Complex partial
41
Q

Types of generalized seizures

A
  • Generalized seizures • Tonic-­‐clonic
  • Absence
  • Myoclonic
  • Clonic • Tonic • Atonic
42
Q
  • Tonic-­‐clonic
  • Absence
  • Myoclonic
  • Clonic
  • Atonic
A 
Tonic - increased tone
Clone - repetative
Absence - forget where they are
Myoclonic - small motor twitch
Atonic - limp & collapse
43
Q

Types of focal seizures

A
  • Sensory
  • Altered consciousness
  • Motor / autonomic signs
  • “Secondary generalizaRon”
44
Q

Things mistaken for seizures

A
  • Syncope: Transitory loss of consciousness, short, no pre-­‐/post-­‐ ictus; cardiac vs respiratory
  • Cataplexy/narcolepsy
  • Neck Pain
  • VesRbular dysfuncRon
  • Metabolic encephalopathy
  • Idiopathic head tremor
  • Generalized tremor syndromes
  • Exercise-­‐induced weakness
  • Compulsive disorders
  • Stereotypy
  • Feline estrus behaviours
  • Myoclonus
45
Q

Genetic epilepsy - what is it? cause? who?

A

Genetic Epilepsy
• Direct result of a known or presumed geneRc defect • Intracranial cause
• Generalized tonic-­‐clonic seizures
• Dogs&raquo_space; cats / horses

46
Q

Genetic Epilepsy - breeds?

A
  • Australian Shepherd
  • Beagle
  • Belgian Shepherd (Tervueren)
  • Bernese Mountain Dog
  • Border Collie
  • DalmaRan
  • English Springer Spaniel
  • German Shepherd Dog (AlsaRan)
  • Golden Retriever
  • Irish Woljound
  • Keeshond
  • Labrador Retriever
  • PeRt Basset Griffon Vendeen • Lagoeo Romagnolo
  • Shetland Sheepdog
  • Standard Poodle
  • Viszla
47
Q

Prognosis for Genetic Epilepsy

A
  • First seizure: 1-­‐5 years of age
  • Normal interictal neurologic exam & diagnosRc tests
  • Prognosis (efficacy of therapy)
  • Breed related
  • Border Collies & Australian Shepherds worse
48
Q

Progressive Myoclonic Epilepsy

A
  • Genetic epilepsy syndromes with progressive neurologic decline over Rme (abnormal interictal neurologic exam)
  • Autosomal recessive
49
Q

Structural/Metabolic Epilepsy

A
  • Signalment does not fit geneRc epilepsy • Breed
  • Age of seizure onset
  • Interictal abnormaliRes found on diagnosRc tests, including neurologic exam
50
Q

What are toxic causes for structural/metabolic epilepsy

A 
Extracranial DDx
•  Toxic: •  Lead
•  Organophosphates •  Ethylene glycol
•  Chocolate
•  Xylitol
51
Q

What are metabolic causes for structural/metabolic epilepsy?

A
  • Hypoglycemia: iatrogenic, young/toy, insulinoma • Organ failure: hepaRc/uremic encephalopathy
  • Electrolyte abnormaliRes: Na+, H2O, K+, Ca2+
  • Hypoxemia
  • Hyperlipidemia
  • Hyperthermia
52
Q

What are intracranial causes for structural/metabolic epilepsy?

A
  • Vascular: hypertension, hyper/hypothyroidism (cats/dogs)
  • Inflammatory/Infec@ous: encephaliRdes: GME, FIP
  • (Bacterial, viral, fungal, protozoal, rickeesial, larval migrans)
  • Trauma@c: head trauma
  • Anomaly: hydrocephalus, cortical dysplasia (e.g. lissencephaly)
  • Idiopathic: geneRc epilepsy
  • Neoplasia:
  • Primary (e.g. meningioma)
  • MetastaRc (e.g. hemangiosarcoma)
  • Degenera@ve:
  • Mitochondrial encephalopathies / storage diseases / organic acidurias
  • Thiamine deficiency (polioencephalomalacia)
53
Q

Unknown epilepsy

A

Truly idiopathic
Signalment does not fit genetic epilepsy
No cause identified on diagnostic tests
How?
* Lesion is beyond the level of detecRon by current technology
• Genetic, just don’t know it yet
• Old trauma (birth? Previous encephalitis?)

54
Q

Signalment for epilepsy causes

Causes based on age (< 1 year, 1-5, > 5 y)

A

Breed
Age
5y
• Neoplasia (primary&raquo_space; secondary)

55
Q

How does history help with determining if it is a seizure?

A

Seizure or not?
• Good descripRon of pre-­‐ictal, ictal, post-­‐ictal behaviour (VIDEO)
• Consciousness?
• DuraRon/frequency/Rme of day (seizures most common
when drowsy)
• Interictal mentaRon, personality

56
Q

5 things in a basic biochem panel to say that the liver is working

A

Liver:
1. Protein (albumin)
2. BUN (makes urea from ammonia in the gut)
3. Bilirubin
4. Glucose: glycogenolysis (glucose will drop)
5. Cholesterol: (LDL, HDL etc)
Clotting factors - but not in a routing biochem

57
Q

Seizure Exam (diagnosis

A 
•  Physical Exam:
•  Rule out non-­‐epilepRc events (cardiac arrhythmia? Neck pain?) •  Rule in extracranial causes (lymph nodes? CyanoRc mm?)
•  Neurologic Exam:
•  DO THE WHOLE EXAM
•  4 tests specific to thalamocortex?
NAF
•  GeneRc (idiopathic) epilepsy •  (Early neoplasia)
Deficits
•  PosRctal
•  Drugs (therapy)
•  Structural/metabolic epilepsy
58
Q

Seizure diagnosis minimum database

A
  • CBC
  • Serum biochemistry profile • 5 tests of liver funcRon?
  • Electrolytes
59
Q

Seizure diagnosis expanded database

A
  • Thyroid panel: TT4, TSH, fT4
  • Blood pressure (note machine, cuff, limb, recumbency, x3) • Toxicology
  • Titres / PCR
  • Thoracic radiographs
  • Abdominal ultrasound
60
Q

Seizure diagnosis advanced database (only if the previous tests are normal)

A

Only if previous tests are normal • EEG: if not sure seizure
• MRI vs CT
• CSF analysis (“spinal tap”)
• Biopsy?

61
Q

EEG

A

Electro encephalogram

62
Q

Treatment - when do you treat?

A
  • Frequent seizures
  • é frequency
  • é severity
  • Status epilepRcus or clusters
  • Structural/metabolic epilepsy: treat the cause
63
Q

Goals of treatment/commitment

A
  • Practical goals of therapy: not seizure eradicaRon
  • decreased frequency & severity
  • Expected adverse effects
  • Commitment
    * Lifestyle: Dosing requirements
    * Cost: Drugs + routine monitoring bloodwork
    * Organization: Seizure dietary to monitor efficacy
64
Q

Treatment - drug choices

A 
Phenobarbital ***
Potassium ***
Bromide 
Levetiracetam 
Gabapentin/Pregabalin
 Zonisamide 
Topiramate (not common)
Phenytoin (not common)
Felbamate (not common)
Diazepam: too short-­‐acRng, tolerance builds up, emergency only
65
Q

When should you monitor how the treatment is working?

A

When to check serum [drug] is within therapeutic range:
• @ steady-­‐state aber starRng Tx or dose Δ
• Uncontrolled seizures despite apparently adequate dose
• @ signs of dose-­‐related toxicity
• Every 6-­‐12 months (to check for pharmacokineRc Δ causing drib)

66
Q

Status epilepticus

A

≥ 30 mins conRnuous/intermieent seizure acRvity • Start Tx ≥ 5 mins conRnuous/intermieent seizures

67
Q

Potential physiologic complicaRons?

A
  • Respiratory, cardiovascular, renal, autonomic, metabolic, neurologic
  • Treatment: supporRve care +
68
Q

Treatment in status epilepticus

A 
Start with top & go down
Diazepam
Phenobarbitol
Propofol
Inhalants
69
Q

Refractory Epilepsy

A
  • QoL compromised by seizure severity or frequency, or medicaRon adverse effects
  • ConsideraRons:
    • Lack of response to 2 drugs
    • ≥1 seizure/mo
    • Duration ≥1yr

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