James - Neurology Flashcards
VITAMINN D - what do the letters stand for?
- 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
What can cause encephalitis (inflammation of the brain)?
Infectious(6)/non-infectious
- 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 - Non-infectious (immune-mediated) - approx 99% in Ontario
What structures are affected with GME? (Granulomatous meningoencephilitis)
Brain, spinal cord, meninges, can be optical (CN II)
What is the breed disposition for necrotizing encephalitis?
Small breeds, younger age (2-5 y)
e.g. pugs, maltese, chihuahua for NME
yorkshire terriers for NLE (Necrotizing Leukoencephalitis)
What is the difference between NME and NLE
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
What is Necrotizing encephalitis?
NME - Cerebral & white matter + meningitis
NLE - Brainstem, cerebral white matter
–> eating away from mild edema
Necrotizing encephalitis - Diagnostic tests
CBC/profile/UA Thoracic rads, abdominal ultrasound MRI (brain +/- spinal cord CSF analysis -> inc. nucleated cells/inc TP Titres, PCRs HIstopathology (definative)
Necrotizing encephalitis - Diagnostic tests for infectious cause suspected
Titres, PCRs
Brain tumours - signalment
Older dogs & cats
Brain tumours - primary (5)? Secondary (2)?
Primary(5): neurons, glial cells(supportive, form myelin), choroid plexus, ependymal (thin membrane lining the ventricles), meninges
Secondary: local extension, metastases
Most common primary brain tumour? Other common ones?
Meningoma
Glioma (astrocytoma, oligodendroglioma, glioblastoma)
Choroid plesus tumour (papilloma vs. carcinoma)
Ependymoma
Secondary Brain tumours - local extension (4)
Local extension: • Calvarial (osteosarcoma, MLO) • Nasal carcinoma • Pituitary tumour • PNST (CN V)
Secondary Brain tumours - metastatic (4)
Metastatic: • HSA (hemangiosarcoma) • LSA (lymphosarcoma) • Carcinoma – mammary, pulmonary, prostatic • Malignant melanoma
Brain Tumours Treatment
Factors for choice
4 options with details
- Factors: tumour type, location, morbidity/mortality, cost
- Corticosteroids
- Chemotherapy: lomustine, hydroxyurea, cytosine arabinoside
- Radiation therapy: linear accelerator, gamma knife
- Surgery
Metabolic Encephalopathies - what parts of the body cause these?
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
Metabolic Encephalopathies - clinical signs
Clinical Signs: • Symmetrical (whole system affected) • ThalamocorTcal • Depression, disorientaTon • Pacing, head pressing • Menace response deficits • Seizures
Examples of congenital disorders
• Hydrocephalus
ly means a smooth brain without evidence
eopallium.
rtical fo•l diAngratochpnrooduidcecgysritsa,ndlysuslcei.nIct eispahaly, etc.
Circling to the right?
Thalamo-cortex, right (Direction they circle in is not contra)
Neurological exam
- MentaTon
- Gait & Posture
- Cranial Nerves
- Postural ReacTons
- Spinal Reflexes
- PalpaTon (Spinal Pain)
Depressed/obtunded - what is it & where is the lesion?
- Drowsiness, inattention, less responsive to environment
- Brainstem (ARAS)
- Thalamocortex
Stuporous - what is it & where is the lesion
- Unconsciousness +êresponsiveness • Can be aroused with noxious sTmulus • ParTal disconnecTon
- Brainstem (ARAS)
Comatose - what is it & where is the lesion
- Unconsciousness + NO responsiveness • Total disconnecTon
- Reflexes may be intact
- Brainstem (ARAS)
Disoriented - where is the lesion
• Thalamocortex &/or vestibulocerebellar
Thalamocortex: NE
- 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
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)
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
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 flowèhydrocephalus
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
EncephaliTs: Clinical Signs
MulTfocal / diffuse CNS • Acute / subacute
• Progressive
What areas are there problems in for the following:
encephalitis
Brain
MyeliTs
Spinal Cord
Meningitis
Meninges
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…
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
What is epilepsy?
Epilepsy: A condiRon of recurrent seizures due to a chronic brain disorder
Prodrome:
Period preceding seizure, consisRng of a change in sensorium of paRent exhibited in behaviour; ~ hrs – days
Aura:
IniRal motor or sensory signs of a seizure; ~ seconds
Ictus:
Seizure itself
Post-‐ictus:
Recovery period with transient abnormaliRes, e.g. mentaRon, menace, gait; ~ minutes – days
Timing of seizures
Singles (self-limited) - Isolated
Cluster - >= 2 in 24, recover in between
Status Epilepticus - continuous
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”
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
Types of generalized seizures
- Generalized seizures • Tonic-‐clonic
- Absence
- Myoclonic
- Clonic • Tonic • Atonic
- Tonic-‐clonic
- Absence
- Myoclonic
- Clonic
- Atonic
Tonic - increased tone Clone - repetative Absence - forget where they are Myoclonic - small motor twitch Atonic - limp & collapse
Types of focal seizures
- Sensory
- Altered consciousness
- Motor / autonomic signs
- “Secondary generalizaRon”
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
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»_space; cats / horses
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
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
Progressive Myoclonic Epilepsy
- Genetic epilepsy syndromes with progressive neurologic decline over Rme (abnormal interictal neurologic exam)
- Autosomal recessive
Structural/Metabolic Epilepsy
- Signalment does not fit geneRc epilepsy • Breed
- Age of seizure onset
- Interictal abnormaliRes found on diagnosRc tests, including neurologic exam
What are toxic causes for structural/metabolic epilepsy
Extracranial DDx • Toxic: • Lead • Organophosphates • Ethylene glycol • Chocolate • Xylitol
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
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)
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?)
Signalment for epilepsy causes
Causes based on age (< 1 year, 1-5, > 5 y)
Breed
Age
5y
• Neoplasia (primary»_space; secondary)
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
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
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
Seizure diagnosis minimum database
- CBC
- Serum biochemistry profile • 5 tests of liver funcRon?
- Electrolytes
Seizure diagnosis expanded database
- Thyroid panel: TT4, TSH, fT4
- Blood pressure (note machine, cuff, limb, recumbency, x3) • Toxicology
- Titres / PCR
- Thoracic radiographs
- Abdominal ultrasound
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?
EEG
Electro encephalogram
Treatment - when do you treat?
- Frequent seizures
- é frequency
- é severity
- Status epilepRcus or clusters
- Structural/metabolic epilepsy: treat the cause
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
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
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)
Status epilepticus
≥ 30 mins conRnuous/intermieent seizure acRvity • Start Tx ≥ 5 mins conRnuous/intermieent seizures
Potential physiologic complicaRons?
- Respiratory, cardiovascular, renal, autonomic, metabolic, neurologic
- Treatment: supporRve care +
Treatment in status epilepticus
Start with top & go down Diazepam Phenobarbitol Propofol Inhalants
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
