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

James - Neurology Flashcards

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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
Cranial Nerves: Tests
* 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)
26
Brainstem: NE
* 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
27
Encephalopathy: Clinical Signs
* 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
28
EncephaliTs: Differentials
* 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
EncephaliTs: Clinical Signs
MulTfocal / diffuse CNS • Acute / subacute | • Progressive
30
What areas are there problems in for the following: encephalitis Brain MyeliTs
Spinal Cord Meningitis Meninges
31
Infectious Encephalitis
* 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
What is a seizure?
Seizure: A transient occurrence of signs due to abnormal excessive or synchronous neuronal acRvity in the thalamus & cerebral cortex (thalamocortex) NeurolocalizaRon: Thalamocortex
33
What is epilepsy?
Epilepsy: A condiRon of recurrent seizures due to a chronic brain disorder
34
Prodrome:
Period preceding seizure, consisRng of a change in sensorium of paRent exhibited in behaviour; ~ hrs – days
35
Aura:
IniRal motor or sensory signs of a seizure; ~ seconds
36
Ictus:
Seizure itself
37
Post-­‐ictus:
Recovery period with transient abnormaliRes, e.g. mentaRon, menace, gait; ~ minutes – days
38
Timing of seizures
Singles (self-limited) - Isolated Cluster - >= 2 in 24, recover in between Status Epilepticus - continuous
39
Generalized Seizure (previously Grand mal)
* 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
Focal Seizures
* 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
Types of generalized seizures
* Generalized seizures • Tonic-­‐clonic * Absence * Myoclonic * Clonic • Tonic • Atonic
42
* Tonic-­‐clonic * Absence * Myoclonic * Clonic * Atonic
``` Tonic - increased tone Clone - repetative Absence - forget where they are Myoclonic - small motor twitch Atonic - limp & collapse ```
43
Types of focal seizures
* Sensory * Altered consciousness * Motor / autonomic signs * “Secondary generalizaRon”
44
Things mistaken for seizures
* 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
Genetic epilepsy - what is it? cause? who?
Genetic Epilepsy • Direct result of a known or presumed geneRc defect • Intracranial cause • Generalized tonic-­‐clonic seizures • Dogs >> cats / horses
46
Genetic Epilepsy - breeds?
* 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
Prognosis for Genetic Epilepsy
* 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
Progressive Myoclonic Epilepsy
* Genetic epilepsy syndromes with progressive neurologic decline over Rme (abnormal interictal neurologic exam) * Autosomal recessive
49
Structural/Metabolic Epilepsy
* Signalment does not fit geneRc epilepsy • Breed * Age of seizure onset * Interictal abnormaliRes found on diagnosRc tests, including neurologic exam
50
What are toxic causes for structural/metabolic epilepsy
``` Extracranial DDx • Toxic: • Lead • Organophosphates • Ethylene glycol • Chocolate • Xylitol ```
51
What are metabolic causes for structural/metabolic epilepsy?
* Hypoglycemia: iatrogenic, young/toy, insulinoma • Organ failure: hepaRc/uremic encephalopathy * Electrolyte abnormaliRes: Na+, H2O, K+, Ca2+ * Hypoxemia * Hyperlipidemia * Hyperthermia
52
What are intracranial causes for structural/metabolic epilepsy?
* 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
Unknown epilepsy
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
Signalment for epilepsy causes | Causes based on age (< 1 year, 1-5, > 5 y)
Breed Age 5y • Neoplasia (primary >> secondary)
55
How does history help with determining if it is a seizure?
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
5 things in a basic biochem panel to say that the liver is working
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
Seizure Exam (diagnosis
``` • 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
Seizure diagnosis minimum database
* CBC * Serum biochemistry profile • 5 tests of liver funcRon? * Electrolytes
59
Seizure diagnosis expanded database
* Thyroid panel: TT4, TSH, fT4 * Blood pressure (note machine, cuff, limb, recumbency, x3) • Toxicology * Titres / PCR * Thoracic radiographs * Abdominal ultrasound
60
Seizure diagnosis advanced database (only if the previous tests are normal)
Only if previous tests are normal • EEG: if not sure seizure • MRI vs CT • CSF analysis (“spinal tap”) • Biopsy?
61
EEG
Electro encephalogram
62
Treatment - when do you treat?
* Frequent seizures * é frequency * é severity * Status epilepRcus or clusters * Structural/metabolic epilepsy: treat the cause
63
Goals of treatment/commitment
* 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
Treatment - drug choices
``` 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
When should you monitor how the treatment is working?
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
Status epilepticus
≥ 30 mins conRnuous/intermieent seizure acRvity • Start Tx ≥ 5 mins conRnuous/intermieent seizures
67
Potential physiologic complicaRons?
* Respiratory, cardiovascular, renal, autonomic, metabolic, neurologic * Treatment: supporRve care +
68
Treatment in status epilepticus
``` Start with top & go down Diazepam Phenobarbitol Propofol Inhalants ```
69
Refractory Epilepsy
* 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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