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Neurological Emergencies Prof. Dr. Çiğdem Özkara.

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Presentation on theme: "Neurological Emergencies Prof. Dr. Çiğdem Özkara."— Presentation transcript:

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 NervesMuscles

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 a)Well demarcated level sensory or motor. b)Sensory dissociation: a) decreased pain on one side,decreased vibration and position on the other side ; b) sensory deficit on one side, motor deficits on the other side a)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-ophtalmologicalDementia 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 HeadacheWeaknessDizzinessSeizures 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

12 Glasgow Coma Scale Eye Opening Spontaneous4 To loud voice3 To pain2 None1 Verbal Response Oriented5 Confused, Disoriented4 Inappropriate words3 Incomprehensible words2 None1 Motor Response Obeys commands6 Localizes pain5 Withdraws from pain4 Abnormal flexion posturing3 Extensor posturing2 None1

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 reflex is 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 diagnosis I. 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 StrokeSeizure –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 HeadacheWeaknessDizzinessSeizures Gait disturbances

22 Headache: Nasty Nine 1. First/ new, severe headache 2. Abrupt onset 3. Progressive and changing pattern 4. Headache with neurologic symptoms>1hr 5. Abnormal neurological findings 6. Headache with syncope and seizures 7. New headaches in children 50 yr 8. New headaches in pregnancy, with cancer, immunosuppression 9. Headaches worsening with exertion, sex, Valsalva maneuver

23 Primary headache syndromes tension-typeClustermigraine

24 Secondary headache syndromes SAHMenengitis 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 HeadacheWeaknessDizzinessSeizures 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 yrs old woman Developed R hemiparesis Medical history: hypertension FE: 170/95mmHg, 115 /min pulse rate NE: R central facial paresis, motor 2/5, 4/5 What is this? Where can be the lesion? What to do?

31 Common neurological Presentations Altered mental status HeadacheWeaknessDizziness 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 Vestibuler Peripheral (inner ear sensory organs, afferents and brainstem efferents,) Peripheral (inner ear sensory organs, afferents and brainstem efferents,) Central (vestibuler nuclei, CNS connections) Central (vestibuler nuclei, CNS connections) Nonvestibuler Nonvestibuler

34 Dizziness

35 Vertigo

36 Nystagmus

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

38 Common neurological Presentations Altered mental status HeadacheWeaknessDizziness Gait disturbances Seizures

39 Hemiparetic Ataxic: dorsal column, cerebellum, peripheral nerve Steppage: foot drop; L5 radiculopathy, peroneal HystericalSpastic Parkinsonian conditions Early gait apraxia: elderly, small uncertain steps Late gait apraxia: dementia; small hesitant steps Waddling

40 Common neurological Presentations Altered mental status HeadacheWeaknessDizziness Gait disturbances Seizures

41 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 !!

42 Causative factors TraumaTumorCVA IC inf. Acute metab. disorder Intoxication Drugs (ciprofloxacin, baclofen, flumazenil..) Mycoplazmosis pneumonia, cat scratch disease encephalitis, HSV6, AIDS, dural metastasis)

43 Types of SE Generalized convulsive SE Epilepsia partialis continua Myoclonic status in coma Nonconvulsive SE –Complex Partial seizures –Absence

44 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

45 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

46 Metabolic and endocrinologic changes Lactic acidosis HypoglicemiaHypo/hyperkalemiaHyponatremia Myoglobunuria or dehydratation acute tubuler necrosis, fulminan renal and hepatic failure Rabdomyolisis is prevented by artificial ventilation and muscle paralysis NorAdr and adrenaline release

47 Other complications Acute pancreatitis Fractures Infections (lung, skin and urinary system) TromboflebitisDehydratationDIC Cerebral venous trombosis Cerebral infarct or hemarroge

48 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

49 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

50 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

51 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

52 17 yrs old girl GTC Seizure on awakening Confused at ER No focal signs History: Birthday party until late night What is this? Where can be the lesion? What to do?

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