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Seizure

Seizure. Dr. Sterczer Ágnes associate professor SZIU, Faculty of Veterinary Science , Internal Medicine Department and Clinic. Seizure Clinical manifestation of an abnormal neuronal hyperactivity involving the cerebrocortical neurons

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Seizure

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  1. Seizure Dr. Sterczer Ágnes associate professor SZIU, Faculty of Veterinary Science, Internal Medicine Department and Clinic

  2. Seizure • Clinical manifestation of anabnormal neuronal hyperactivity involving the cerebrocortical neurons • PATHOPHYSIOLOGY:imbalance between normal excitatory and inhibitory mechanisms • Prodrome: (before seizure). Hiding, attention seeking, whining, agitation • Aura: (initial manifestation of seizure) stereotypical sensory /motor activity: pacing, licking, swallowing. Barking, attention seeking • Ictus: (seizure itself) loss/derangement of consciousness, altered muscle tone, jaw chomping, salivation, involuntary urination, defecation • Postictal period: (disorientation, somnolence, altered thirst etc)

  3. SEIZURE CLASSIFICATION • IDIOPATHIC EPILEPSY • primary, idiopathic (genuine) epilepsy • Functional intracranial • no obvious structural brain disease • SECONDARY SEIZURE or EPILEPSY • Structural diseases of the brain • structural brain damage caused by infections, trauma,brain malformations, tumors etc. • REACTIVE SEIZURE • Extracranial disease • Normal brain • GENERALIZED • PARTIAL (focal) • simple • complex

  4. GENERALIZED seizure • widespread onset within both cerebral hemisphere • loss of consciousness • recumbence • generalized motor signs, mostly violent motor activity that involves the whole body (convulsions) Tonic (sustained), clonic (repetitive) contractions, limb paddling and trembling, jaw chomping, facial twitching • Autonomic hyperactivity: pupillary dilatation, salivation, piloerection, micturiation, defecation • Metabolic diseases, toxicosis, IE

  5. GENERALIZED: videó videó

  6. Partial / Focal • focal onset in one cerebral hemisphere • focal acquired structural brain lesion • Aura (initial portion of seizure) • postictal motor deficit (transient localized loss of motor function) • Psychomotor seizures (bizarr behaviors) • Simple partial:neocortical structures of one hemisphere • no consciousness alterations! • unilateral motor signs on contralateral to side of the seizure focus • Facial twitching, • Tonic or clonic movements of one limbs • Spasmodic turning of the head to one side

  7. PARTIAL / FOCAL (petit mal) • focal onset in one cerebral hemisphere • focal acquired structural brain lesion • Complex partial:allocortical structures and often continues bilaterally • Focal seizures progress to generalized motor seizures • Consciousness impared or loss! • contralateral or bilateral asymmetric or symmetric motor signs limited to some parts of the body • circling, behavioral activities like startling, growling, hissing, chasing often seen in cats • Bizarre activity may be seen (psychomotor seizures) • Stereotypical (circling) • Behavioral (startling, growling, hissing, chasing, attacking objects, fly biting, howling)

  8. Petit mal: videó

  9. SEIZURE • Isolated seizure • Brief, isolated event, lasting<2 min) • „Cluster” seizures • >2 over 24-hour period • Status epilepticus: • Neurologic emergency! • continuous clinical seizures lasting at least 10 minutes • seizures repeated at brief intervals for >30 minutes without complete recovery of consciousness between individual attacks • Convulsive (generalized violent motor activity) • Nonconvulsive (milder, subtle motor signs) • >20 min irreversible neurologic damage

  10. Common disorders resulting in seizures EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia) IDIOPATHIC EPILEPSY

  11. EXTRACRANIAL reasons • Reactiv epileptic seizures • Alter the brain biochemical homeostasis in favor of excitation • Endogen/exogen neurotoxins→blood –brain barrieror neurotransmission • CS /SE • Rapidly recurring seizures may recruit adjacent areas of brain and may produce neuronal damage • Consciousness can be changed • confusion, delirium, depression

  12. EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,chlorinated hydrocarbons, metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia)

  13. Strychnine • Stiff extension of legs and body, tetanic spasms induced by auditory stimuli • emesis (if no neurologic signs), gastric lavage, pentobarbital • Metaldehyde • Snail, rat poison • Hyperesthesia, tachycardia, salivation, tremor, nystagmus in cat, respiratory failure, seizure, (not worsened by auditory stimuli) • Acetaldehyde odor on breath • Gastric lavage, intubation, ventilation, pentobarbital • Organophophates, carbamates • insecticides • Salivation, lacrimation, GI, miosis, twitching facial and tongue muscles, tonic-clonic seizures • signs+low serum acetylcholinesterase activity • Atropine 0,2 mg/kg iv  sc 3xpralidoxime 20 mg/kg im 2x if <48h or dermal exposure

  14. TOXICOSIS-SEIZURE • Chlorinated Hydrocarbons • Insecticids, agricultural products, absorbed through skin • Hypersensitivity, salivation, muscle twitching of face and neck, tremor, tonic-clonic seizures • Insecticide smell to haircoat • Wash with warm, soapy water, pentobarbital • Lead • Abdominal pain, GI, megaesophagus, hysteria-aggression, tremor, seizure, blindness, hypermetria, nystagmus, dementia • Rbc:basophylic stippling, nucleated rbc , PB>50 mg/dl • Ca-EDTA 25 mg/kg iv 4x (10 mg Ca-EDTA/ml in 5% dextrose) + diuresis! • Succimer 10 mg/kg per os 10-14 day • Ethylene glycol

  15. Metaldehid ethylenglycolvideo

  16. EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,chlorinated hydrocarbons, metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia)

  17. Hypoglykaemia • Sepsis! • Young puppy • Glycogen store and impaired metabolism, ascariosis, fasting • „Toy breed” • Glycogen store, stress, fasting, diarrea • Hunting dogs • Stress, fasting • Hyperinsulinaemia • Treatment of Diabetes mellitus • Insulinoma or other insulin secreting tumors • Very severe liver function injury

  18. EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,chlorinated hydrocarbons, metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia)

  19. Hepatic encephalopathy • Encephalopathy due to liver failure. Syndrome Acut (6-8%) rare • acut, fulminant encephalopathy severe liver necrosis(70-80%) • severebrain oedema (glutamin accumulation in the brain) Chronic HE 92-94 % common • PSS collateral circulation + decreased liver function! • Portosystemic encephalopathy (PSE) • congenital/acquaried PSS • Cat: Hepatic lipidosis; congenital enzim deficiency of urea c. • Failure of the neurotransmitter systems

  20. Hepatic encephalopathy Symptom • Episodic, reversible (CPSS), • GI:anorexia, weight loss, vomitus, diarrhoea, salivationAPSS: more expressedGI: portal hypertensionascites, oedema, melaena • Urinary system signs 40-50%PU/PD, urat urolithiasis, cystitis, dysuria, stranguria, pollakisuria haematuria, cristalluria, ammonium-biurat crystals • CNSsigns 80-90% 1-4 grade! • Severness not correlate with the ammonia level • Episodic, wavy intensity, severity Diagnosis • Labor: microcytosis (CPSS), liver enzymes /, urine: ammonium-biurat crystals (CPSS) • Liver function tests: NH3 (ATT, PPATT) ; FBA-PPBA • CPSS: doppler US, (scintigraphy, porthography)

  21. Hypokalaemia-alkalosis IC EC K↓ K K H+, Na+ acidosis alkalosis NH3+ H+↔ NH4+

  22. EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,chlorinated hydrocarbons, metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia)

  23. hypocalcaemia

  24. EXTRACRANIAL DISORDERS 1. Toxins(Pb, etylenglycol, org.P,chlorinated hydrocarbons, metaldehyd, strychnin) 2. Metabolic diseases 2.1. Hypoglycaemia 2.2. Liver diseases HE 2.3. Hypocalcaemia 2.4. Severe uraemia 2.5. Heat stroke 2.6. Diabetic ketoacidosis 2.7. Electrolyte disturbances 2.8. Hyperlipoproteinaemia 2.9. Hyperviscosity (polycitemia)

  25. Neurologic manifestation of systemic disease • Alteration in electrolyte and water balance • Secondary cerebrocortical dysfunction • Na ↑↓ brain osmolality • Ca ↑↓; K ↑↓ effect on ion channels in CNS, lead to excitatory or inhibitory neurotransmission • Metabolic disorders • Secunder effect on cerebrocortex /thalamusra • Endogen neurotoxins • Polycythemia • ↑viscosity→↓microcirculation→local hypoxia

  26. INTRACRANIAL DISORDERS(CNS) 1. Congenital 1.1. Hydrocephalus 1.2. Lissencephaly 1.3. Cortical dysplasia 2. Neoplasia 3. Inflammatory disease 3.1. Infectious inflammatory disease 3.2. Non infective encephalitis (GME, SRMA.) 4. Vascular disease 4.1. Hemorrhage (coagulopathy, hypertensio) 4.2. hypoxia 4.3. ischaemia 5. Trauma-scar formation 6. Metabolic storage diseses 7. Degenerative conditions

  27. HYDROCEPHALUS • Cerebral ventricular system is enlarged sec. to CSF compression or atrophy of surrounding neurologic tissue. (ICP) Mostly congenital -enlarged head, palpably open fontanelles -episodes of abnormal behavior/dementia/ cortical blindness, divergent strabismus -tetraparesis/decreased proprioceptions • Diagnosis: signs/breed/age/ US/ CT/ EEG

  28. LISSENCEPHALY • Sulci and gyri fail to develop normally  smooth cerebral cortex • rare! • Lhasa Apso (wirehaired Foxterriers/Irish Setters • Clin: behavioral abnormalities, visual deficits, difficult to train, seizures • Diagnosis:EEG,MRI, Brain biopsy(slow wave, high voltage over areas of cerebral cortex)

  29. NEOPLASIA • Gradual onset of slowly progressive neurologic signs.ICP • Acute signs:if hemorrhage/edema occurs association with tumors • Clin:decreased/abnormal response to stimuli, progressive loss of consciousness, change in mentation, dull, depressed, „suddanly old”, seizures, evidence of focal neurologic lesion, circling • Diagnosis: CT/ MRI/ X-ray/ liquor CSF: pressure, tumor cell no, CSF cell count, 50-150 WBC/ul mononuclear, protein (alb+ ,  globulin tumor) (alb+  globulin inflammation)

  30. INFLAMMATORY DISEASES • Inflammation encephalitis seizures • INFECTIOUS inflammatory CNS -acute distemper -FIP-bacterial -FIV-toxoplasmosis -rabies-neosporiosis -Lyme disese-cryptococcosis -Ehrlichiosis-Rocky Mountain spotted fever • FIP CSF:nonseptic inflammation, protein, neutrophil, macrophag, lymphocyta • FIV CSF:protein,lymphocyta,FIV antibody

  31. STEROID-RESPONSIVE-MENINGO-ARTERITIS SRMA • Beagle pain, necrotizing vasculitis, aseptic meningitis • Idiopathic reason, immunological causevasculitis/arteritis affecting meningeal vessels of spinal cord, brainstem • Young dogs (6-18 months) rarely middle-aged • Large breeds most commonly (beagle, boxer, german shorthaired pointers, retriever, Bernese Mountain dogs) • Clinical signs:fever, cervical rigidity, wax and wane vertebral pain • Acut: ≈meningitis chronic: ≈ spinal cord signs • Concurrent immune-mediated polyarthritis (IMPA) • Labor: neutrophil leucocytosis CSF: protein, >100 cells/ul; >75% ngr • High IgA in CSF and blood (acute: ngr, chronic: ly pleocytosis) • Prednisolon  CSF normal or mononuclear cells • CSF should be collected before therapy • Systemic IgA productionDD: GME IgA, IgM produced by nervous s. • Therapy: corticosteroid tapering • If not respond + azathioprine • Prognosis: good

  32. GRANULOMATOUS MENINGOENCEPHALITIS (GME) • Idiopathic inflammatory disorder of CNS in dog • Young, adult dogs 2-6 years (Cat NO) • small breeds (poodles, terriers) • focal/ disseminated/ ocular forms -neurologic dysfunction, severe pain, cervical pain, -brain stem signs: nystagmus, head tilt, blindness, VII, V paralysis, -ataxia, seizures, circling, behavior change • inflammatory cell accumulation/proliferation around blood vessels in CNS (perivascular cuff) • CSF: protein ( globulin), /  pleocytosis ly/mo • First exclude the infective causes of ME!! • CT contrast enhances mass, dg: biopsy • corticosteroid prednisone (cytostatic)

  33. NECROTIZING MENINGOENCEPHALITIS (NME) • Idiopathic inflammatory disorder of brain in Pugs • Necrotizing leucoencephalitis, pug encephalitis • Pug, Malteses, Yorkshire Terriers • no infective agent, genetic predisposition • Necrosis, nonsuppurative necrotizing meningoencephalitis • Progressive cerebral cortical disease • Seizure, neurologic signs referable to cerebrum and meninges • CSF:protein, nucleated cell count, ly • No specific treatment • Prognosis: poor

  34. FELINE POLIOENCEPHALOMYELITIS • nonsuppurative encephalomyelitis • idiopathic • young, adult cats 3 months-6 years -chronic, progressive seizures -spinal cord signs: pelvic limb hyporeflexia ataxia/ paresis of pelvic limbs -intention tremors of the head -behavior change • CSF:protein / mononuclear cells • Definitive diagnosis: necropsy perivascular cuffing with mononuclear cells, ly meningitis, glial nodules, demyelinisation • poor prognosis

  35. FELINE ISCHEMIC ENCEPHALOPATHY FIE • Cerebral infarct syndrome of unknown etiology • middle cerebral artery • summer months adult cats • peracute onset of asymmetrical neurologic abnormalities: • dementia/aggression/circling /seizures/ • proprioception, reflexes in the limbs oppo. • cortical blindness (blind, normal pupillary light reflexes) • acute onset of nonprog. unilateral cortical diseases, no history of trauma or illness

  36. EPILEPSY Syndrome of recurrent seizures, not associated with progressiveIC a) idiopathic/ primer epilepsy • inherited functional problem in the brain b) acquired epilepsy • cerebral insultresidual brain damage Status epilepticus:life-threatening conditionneuronal damage, systemic complication

  37. IDIOPATHIC EPILEPSY • Most common cause of seizures(Cat uncommon) • repeated episodes of seizures with no demonstrable cause. Normal between seizures. Seizure threshold ↓ • Inherited:LABRADOR, RETRIEVERbreedpredisposition: Golden retriever,German shepherd, Belgian Tervuren, Keeshond, Beagle, Dachshund, retrievers, collie, irish setter • 6 m-5 years (juvenile:8-12w---outgrow by 4-6m) • generalized! tonic-clonic seizures • 90% unconsciousness (+psychomotor signs: agression, pacing, hallucination, stargasing, tailchasing) • recur at regular intervals • with aging frequency/severity of seizures • NORMAL:physical/neurologic/ophtalmologicclinicopathologic tests/ CSF/ interictal EEG • Prodromal: aura/preictus-ictus-postictus

  38. ACQUIRED EPILEPSY prior inflamm./traumatic/toxic/metabolic/vascular INSULT alters a focus of neurons seizure • Usually frontal/temporal lobe • Usually partial! Seizure (no uncosciousness) • any age/ any breed, either gender dogs/cats • usually can not be determined the cause • ABNORMAL:physical/neurologic/ophtalmological/clinicopathologic tests/ CSF • EEG may be abnormal • No prodromal phase (aura/ictus) • Progressive: seizures more frequent/intens/longer

  39. DIAGNOSIS Seizures

  40. Nationale • Species, breed, age, sex • History/ Decursus • vaccination, toxin, trauma, drugs, other previous diseases • seizure: form, type,description (video), onset, duration, frequency, present before, day time, signs between two seizure • Other complains, clinical signs • Physical-Ophthalmological-Neurological examination • mm, BCV (temperature, pulse, breathing) • Emergency neurology: consciousness, pupil (size, PLR, symmetricy), eye position, nystagmus, motor function (posture, position of head, ataxia, paresis, reflexes) cranial reflexes, skull, ear • Respiratory alterations • Labor examinations (screening test) • Instrumental examinations

  41. Laboratory test (screening tests) • Next the animal: blood glucose!!!! cystocentesis • CBC (qualitative, quantitative) • Usually not characteristic • leucocytosis-inflammatory diseaseleucocytosis left shift-bacterial meningoencephalitislymphopenia-acute viral infectionmicrocytosis with or without thrombocytopenia- PSS • Biochemistry • Liver: ALT, GGT, ALP, BA, (NH3), TP, alb • Kidney: Urea, creatinine, P • Ionogram: Ca, K, Na acid-base • Serology • serologic tests (FeLV/FIV, distemper, toxoplasma) • Immunology (?) • IC, ANA

  42. Laboratory tests • Urinalysis:-specific gravidity-protein-glucose-ketone-crystalls: • Oxalat: ethylenglycol-toxicosis • ammonium biurate: PSS

  43. Instrumental examinations • CSF (liquor)colour, átlátszóságprotein, enzyme activityglucose, electrolytecell numbermicroorganismsContraindikation:coagulopathy, increased ICP

  44. Instrumental • US:brain, abdomen (liver, kidney, pancreas) • X-Ray • EEG • CT • MR

  45. TREATMENT Status epilepticus ICP

  46. STATUS EPILEPTICUS • Series of seizures without periods of intervening consciousness • medical emergency immediate seizure control is required!seizure>20’ result in permanent neuronal damage • systemic effects of status epilepticus: -hyperthermia -lactic acidosis -hypoxemia -cardiac arrythmias -pulmonary edema -death

  47. Treatment – in seizing animal in status epilepticus • Iv catheter insert Immediately stop ongoing seizures • Diazepamiv. (0.5-1,0 mg/kg dog 0.5 mg/kg cat) • If 2-3’ not effect→ repeat 2-4x 10’ max 3 mg/kg • 2 mg/kg rectally if not iv catheter • Maintain airway, intubation, oxygen, hyperventilation • Pentobarbital-Na(5-15 mg/kg iv. slowly, to effect) • If diazepam not effective repeatedly, or seizure reoccur • Propofol(1-4-(8) mg/kg iv slowly, to effect) • Temperature 38-39.5C • ICP • Blood sampling

  48. Treatment – in seizing animal in status epilepticusban Prevent seizure recurrence over following hours • Phenobarbital(2-4 mg/kg iv/im 2x) • Loading dose: 15-25 mg/kg [PB=80-110 umol/l] • Maintain dose (2-2.5 mg 2x) • Diasepam inf. (0.5 mg/kg/h in salsol inf (KBr!)) • Adsorbed to plastic, inactivated by light, prepare only 1-2 hours solution • If >20’ since last bolus, start with bolus again beginning of infusion, than maintained by infusion • If no seizure for 4-6 h →↓ 25% dose /4-6 h • If >2 seizure during infusion→bolus, ↑1.5 mg/kg/h inf • If inf not possible: 0.5 boluses iv q20’ 4-5x • Pentobarbital inf(2-5 mg/kg/h iv slowly, to effect)

  49. Treatment – in seizing animal in status epilepticusban Control refractory seizures • Propofol • Loading dose: 1-3.5 mg/kg to effect • Maintenance infusion (0.01-0.25 mg/kg/min 6-24 h • General anesthesia • Propofol:bolus 4-6 mg/kg →maintain 0.1-0.3 mg/kg/min • Isofluran • Pentobarbital iv bolus 2-5 mg/kg →maintain 5 mg/kg/h • Monitoring:intubation, respiration, ventilation, hypotension Treatment of CS at home • Rectallydiazepam 1 mg/kg (2. seizure/12-24h) 3-4x repeated q 20’. If >2 seizure recur despite this treatment →hospital

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