Neurological Emergencies

1. Neurological Emergencies Prof. Dr. Çiğdem Özkara

2. Goal of an emergent Neurological Examination • Is there a neurologic condition ? • Where is (are) the lesion(s) located ? • What are the possible causes? • Can the patient discharged from ER safely or is hospitalisation needed ?

3. Anatomical basis of NE • Brain • Brain stem • Spinal cord • Nerves • Muscles

4. Anatomical basis of NE • Brain • Alteration of thought process or consciousness, • Seizures, involuntary movements • Motor and sensory deficit on the same side

5. Brainstem • Cranial nerve deficits in association with motor and sensory deficit • Diplopi, vertigo, dysartria, dysphagia,disequilibrium

6. Nerves • Motor and sensory deficits • Reflex absent or decreased • Findigs limited to nerve root or spesific nerve • Distal symptoms prominent than proximal • Muscles • Weakness (bilat and simm prominent) • Sensation usually normal • Reflexes generally preserved

7. Spinal cord • Well demarcated level sensory or motor. • Sensory dissociation: • decreased pain on one side,decreased vibration and position on the other side; • sensory deficit on one side, motor deficits on the other side • Mixed upper and lower MN

8. Spesific conditions presenting as emergency • CVA (cerebro vascular accedant) • Infections • Movement disorders • PNS (polyneuritis) and neuromuscular disorders • Guillain-Barre Synd. • Myastenia Gravis • Musculoscletal and neurogenic pain • Multiple Sclerosis • Neuro-ophtalmological • Dementia • Brain tumors • Increased Intra Cranial Pressure and herniation synd. • Normal pressure hydrocephalus • Nontraumatic spinal cord emergencies • Sleep disorders

9. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Seizures • Gait disturbances

10. Altered mental status • CNS dysfunction; global, diffuse, bilateral hemispheric, unilateral hemispheric with brain stem impairment (i.e.compression) or primary brainstem dysfunction • Function; • decreased: coma, coma like states • Increased: delirium

11. Coma • Coma can be described as an eyes closed unresponsive state. • Obtundation: a blunting of consciousness • Stupor: a sleep like state from which the patient can be aroused by vigous stimulation • Delirium: Other end of the spectrum with agitation, hallusinations and excessive motor and verbal activity

13. Coma like conditions • Locked-in state: patient is alert, lost all voluntary control except for extraoculer eye movements (basis pontis) • Akinetic mutism: bilateral, deep, medial frontal lobe disease;awake attentive state devoid of verbal or motor output • Vegetative state: Chronic state of unresponsiveness, intact sleep-wake cycles , appear to be awake

14. Evaluation • Abnormal Vital signs: heart rate (atrial fibrill, ventriculer tachycardias; embolic, ischemic…) blood pressure ( hypertensive encephalopathy, ICH,stroke), fever (menengitis, encephalitis, heat stroke..)etc • Respiratory abnormalities: • Cheyne- stokes: bi-hemispheric(ischemic, metabolic) • Hyperventilation: hypothalamic rostral midbrain • Apneustic:mid-lower pontine • Ataxic: medulla

15. Focal neurologic findings: Brainstem reflexes: Pupillary reflexis resistant to metabolic insult , presence of pupillary dysfunction of asymmetry distinguish structural from metabolic coma !!!! ( generally small reactive) There are pharmacologic agents affective: Opiates: pinpoint, poorly reactive pupils Barbiturates: variaus sized relatively fixed Third nerve, sympathetic pathways, ..

16. Ocular reflexes; oculocephalic and oculovestibuler lie adjacent to brainstem areas critical for maintenance of consciousness Motor response

17. Differential diagnosisI.Cerebral dysfunction without focal signs • Trauma • Metabolic encephalopathies • electrolyte, glycemia.. • Organ involvement ; hepatic/ amonnia, renal/urea, endocrine/ myxedema, Addison’s • Hypertensive • Toxic: CO, alcohol, opioids • Nutritional • Postictal (seizures) • Anoxic/hypoxic • Environmental (hypo/hypertermia)

18. II.Cerebral dysfunction with focal signs • Stroke • Seizure • Postictal • Nonconvulsive SE • Trauma • Intra Cranial infections • Intoxications

19. 32 yrs man • Sudden severe headache, vomiting, • GTC seizure on the way to the hospital • PE: tachicardia, fever, sweating • NE: Confused, agitated, meningeal irritation signs: + • What is this? • Where can be the lesion? • What to do?

20. Pearls Evaluation and management will go on at the same time Focal localising signs were described in drug overdoses and metabolic coma !!!

21. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Seizures • Gait disturbances

22. Headache: Nasty Nine • First/ new , severe headache • Abrupt onset • Progressive and changing pattern • Headache with neurologic symptoms>1hr • Abnormal neurological findings • Headache with syncope and seizures • New headaches in children <5yr,>50 yr • New headaches in pregnancy, with cancer, immunosuppression • Headaches worsening with exertion, sex, Valsalva maneuver

23. Primary headache syndromes • tension-type • Cluster • migraine

24. Secondary headache syndromes • SAH • Menengitis • Intracranial mass lesions • Cerebro Vascular Disease • Inflammatory disorders • Disorders of CSF volume and flow (hydrocephalus, pseudotumor cerebri, intracranial hypotension)

25. Pearls • Focus on the new or different headaches not merely the worst • Suspected SAH needs CT and LP • New or different headaches over 50 , suspect temporal arteritis, investigate sedimentation rate

26. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Seizures • Gait disturbances

27. Evaluation of Weakness • Onset: • Acute; initial manifestation of newly onset disease, • Exacerbation of a known progressive; Myastenia Gravis • Slowly progressive; Amyotrophic Lateral Sclerosis • Location • Proximal • Distal • Cranial • Associated symptoms: pain, cramp, GIS(intox: bot) • Medical history

28. Muscle weakness • Cerebral hemispheric lesions: stroke,tm • Spinal cord disordes: tm, inf, disc, • Anterior horn cell disorders: ALS • Nerve root disorders: Guillain-Barre S. • Neuromuscular junction disorders: MG, bot • Myopathies:

29. The most serious presentation of severe muscle weakness“Acute Neuromuscular respiratory failure” Form of restrictive pulmonary disease • Myastenia gravis • Guillain-Barre syndrome • Amyotrophic lateral sclerosis

30. 65 yrsoldwoman • Developed R hemiparesis • Medicalhistory: hypertension • FE: 170/95mmHg, 115 /minpulse rate • NE: R centralfacialparesis, motor 2/5, 4/5 • What is this? • Where can be thelesion? • Whatto do?

31. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Gait disturbances • Seizures

32. Dizziness : the disturbed sense of well being usually perceived as an altered orientation in space Vertigo: illusion of movement of oneself or one’s surroundings

33. Dizziness • Vestibuler • Peripheral (inner ear sensory organs, afferents and brainstem efferents,) • Central (vestibuler nuclei, CNS connections) • Nonvestibuler

34. Dizziness

35. Vertigo

36. Important vestibuler system disorders • Benign positionel vertigo • Vestibuler neuritis • Lbyrinthitis • Meniere’s disease • Cerebello pontine angle tumors • Vascular disease

37. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Gait disturbances • Seizures

38. Gait disturbances • Hemiparetic • Ataxic: dorsal column, cerebellum, peripheral nerve • Steppage: foot drop; L5 radiculopathy, peroneal • Hysterical • Spastic • Parkinsonian conditions • Early gait apraxia: elderly, small uncertain steps • Late gait apraxia: dementia; small hesitant steps • Waddling

39. Common neurological Presentations • Altered mental status • Headache • Weakness • Dizziness • Gait disturbances • Seizures

40. STATUS EPILEPTICUS is recurrent seizures without complete recovery of consciousness between attacks or continuous seizure activity for more than 30 minutes with or without impaired consciousness. • Do not start medication unless the seizure is SE !!

41. Causative factors • Trauma • Tumor • CVA • IC inf. • Acute metab. disorder • Intoxication • Drugs (ciprofloxacin, baclofen, flumazenil..) • Mycoplazmosis pneumonia, cat scratch disease encephalitis, HSV6, AIDS, dural metastasis)

42. Types of SE • Generalized convulsive SE • Epilepsia partialis continua • Myoclonic status in coma • Nonconvulsive SE • Complex Partial seizures • Absence

43. Tonic clonic SE pathophysiology • Motor activity • EEG • Physiological changes • 1. phase: Compensation: SEizure activity increases cerebral metabolism,blood flow increases to compansate the situation. • Blood pressure increase, cardiac output and rate increase, autonomic features (sweating, hypertermia, bronchial secretion, salivation,vomit ) Hyperglicemia

44. Phase 2 • Decompansation: cerebral autoregulation progressively worsen, cerebral blood flow (CBF) depends on systemic blood pressure and hypotension occur, (IV AED HypoTA ) • Systemic and cerebral hypoxia, pulmonary hyperTA, eodema, cardiagenic arrytmia very often • left vent cont card output Cardiac failure • IC pressure syst pre CBF impair EODEMA

45. Metabolic and endocrinologic changes • Lactic acidosis • Hypoglicemia • Hypo/hyperkalemia • Hyponatremia • Myoglobunuria or dehydratation acute tubuler necrosis, fulminan renal and hepatic failure • Rabdomyolisis is prevented by artificial ventilation and muscle paralysis • NorAdr and adrenaline release

46. Other complications • Acute pancreatitis • Fractures • Infections (lung, skin and urinary system) • Tromboflebitis • Dehydratation • DIC • Cerebral venous trombosis • Cerebral infarct or hemarroge

47. General approach • A) 1. step (0-10.min): cardiorespiratory, airway, O2 • B) 2. step: (1-60 min): • 1)follow the neurological status, heart rate, blood pressure, fewer, blood gases, pH, coagulation, haematology • 2)IV AED • 3)IV NaCl 0.9, don’t mix up the drugs, venous lines used for AEDs (trombosis, flebitis..) • Glucos, blood gas, renal and hepatic functions and Ca, Mg,haematology, coagulation, AED levels • 50ml %50 glucose (hypoglisemi), alcoholism, nutritional disorders. Thiamin 250mg IV

48. 3. Step (1-60/90 min) • Etiological investigation ie, AED stopped ? • To treat physiological abnormalities and complications : hypoxia, ICB increase, pulmoner eodema and hyperTA, arrytmia, cardiac failure, lactic asidosis, hyperpirexia, hypoglisemia, elektrolit imbalance, renal or hepatic failure, DIC, rabdomyolisis • HypoTA : pressor treatment: dopamin 2-5 micgr/kg/min, IV monitor • 4. Step (30-90.min): ICU

49. AED administration • A) prodromal phase: diazepam (10mg IV,2-5mg/min,repeat after 15 min, rectal), midozolam, paraldehid, clonozepam • B) early SE: (0-30min) diazepam, midozolam,clonazepam (1mg/30sn) • C)persistance SE(30min<): physiological decompensation, phenobarbitone 10mg/kg 100mg/min and/or Pht 15-20mg/kg 50mg/min • D) Refractory SE(60-90min): anestesia

50. Management of a patient during a seizure • Bend towards left side • Avoid to injure himself • Touch gently • Never place anything in his mouth unless you see them in the beginning • Stay with him until he recovers