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Dr. Boroumand
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Cortex: Awareness (HCF) Brain Stem: Awakeness = ARAS Posterior Fossa
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Full Awake(alert) Drowsiness Stupor Coma Acute Confusional States Or Delirious State
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Pathologic Sleep
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Brain Stem: 1-Awakeness 2-Respiration 3-Eye Fixation 4-Sleep Cycle 5-Weight gain 6-Yaupping 7-Cardiac Rhythm 8-Bilateral Long Tract Pathways (Hemi to Tetra paresis) Posterior Fossa
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Means : Cortex (off) + Brain Stem (on) (cortical Death) Loss of Awareness Duration > 6 m/o = PVS
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Localization : Bilateral Ventral Pontine Lesions Quadriplegia + Lower Cranial Nerve Palsy Causes: 1- Pontine Stroke 2- CPM 3- MS 4- ALS 5- Alzhiemer’s Disease 6- GBS 7- NMJ-Blockers Drugs 8- Brain stem lesions (Lymphoma-Glioma- TB- Syphilis)
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Syn.: Irriversible Coma Cortex off + Brain Stem off + Obvious Lesion + Irriversible Damage Obvious Lesion Means: Bilateral Cortical Damage or Structural Lesion in BS In Brain Death: EEG is flat
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کرایتریای مرگ مغزی : بیمار در کوما باشد عدم وجود تنفس خودبخودی فقدان رفلکس های ساقه مغزی سکوت در EEG فقدان جریان خون مغزی فقدان هرگونه علت برگشت پذیر مغزی مانند مسمومیت با فنوباربیتال Irriversible Coma = Brain Death
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Cortex Off Brain Stem Reflexes off EEG is completely Flat BUT: Obvious lesion (-) CT and MRI (NL)
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Forced Alkaline Diuresis
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↓ in LOC means: 1- Bilateral Cortical Damage 2- Brain stem Structural Damage 3- Unilateral Supratentorial Damage extending toward the brain stem or the other Side
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Full Awake(alert) Drowsiness (Normal Stimulation) Stupor (Painfull/Forcefull Stimulation) Coma (Unresponsiveness) or Loss of Verbalization
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EEG ∝ ↓LOC EEG can determine the level of consciuosness
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Attention Concentration Acute Confussional State ( ↓ LOC) : No At. + No Con. Dementia : Attention Ok + No Concentration Dementia: ↓ in COC ( not: ↓ in LOC)
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caused by: impaired cerebral perfusion (syncope, fainting), cerebral ischemia, migraine, epileptic seizures, metabolic disturbances, sudden increases in intracranial pressure sleep disorders.
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Syncope may result from: 1. Cardiac, 2. Noncardiac 3. Undetermined causes
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decreased cardiac output secondary to cardiac arrhythmias, outflow obstruction, hypovolemia, orthostatic hypotension, decreased venous return
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Cerebrovascular disturbances due to: transient ischemic attacks of the posterior or anterior cerebral circulations, cerebral vasospasm from migraine, subarachnoid hemorrhage hypertensive encephalopathy
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Absence seizures Generalized tonic-clonic seizures Complex partial seizures
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Cardiac encephalopathy, hepatic encephalopathy, uremia, hypoglycemia, hypoxia, hyponatremia, hypo-/hypercalcemia, hypo-/hypermagnesemia, other electrolyte disturbances toxic and industrial exposures (carbon monoxide, organic solvent, lead, manganese, mercury, carbon disulfide, heavy metals)
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LOC Detection 6 Step Assessment IV-Line x2 TNG ECG Dizepam Refer to Specialist
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موفق باشید
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Dr. Boroumand
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تعداد و نوع سردرد نحوه شروع سردرد فرکانس و پریودیسیتی سردرد چقدر طول می کشد تا سردرد به اوج خود برسد عوامل تریگر سردرد کدامند درد از کجا شروع می شود و چگونه پیشرفت میکند. مداوم است یا ضرباندار آیا پیش درآمدی برای شروع سردرد هست یا خیر عوامل تشدید کننده سردرد عوامل تخفیف دهنده سردرد کدامند. خود بیمار چه ایده ای از علت سردرد خود دارد.
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Definition: 1. American Academy of Neurology guidelines as a one-month interval. 2. a 6- to 12-month interval.
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An increasingly severe headache, Change for the worse in an existing headache pattern all means the possibility of an expanding intracranial lesion.
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Means an intracranial hemorrhage, usually in the subarachnoid space but also can be caused by : intracerebral hemorrhage, cerebral venous thrombosis, Embolic cerebellar infarction arterial dissection, pituitary apoplexy, spontaneous intracranial hypotension, benign angiopathy of the central nervous system (CNS), (reversible cerebral vasoconstriction syndrome) acute hypertensive crisis, idiopathic “primary thunderclap headache”
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Explosive Severe Exertinal Resistant Usually with no focal neurological signs (unless 3th nerve plasy, …) Papilledema and subhyaloid hemorrhage. Neck stiffness
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Female Hypercoagulability state (dehydration, OCP, pregnancy, delivery) Gradual increasing headache but sometimes suddenly onset. Resisitant to treatment May have focal neurological signs.
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A history of antecedent head or neck injury should be sought; even a relatively minor injury can be associated with: 1. the subsequent development of epidural, subdural, subarachnoid, or intraparenchymal hemorrhage 2. posttraumatic dissection of the carotid or vertebral arteries
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1. A primary headache disorder unassociated with structural disease 2. can be associated with migraine BUT These must be excluded with the first occurrence of such headaches. Subarachnoid hemorrhage Arterial dissection, which
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Commonly manifests with: 1. Neck, face, and head pain ipsilateral to the dissection, 2. Frequently is associated with an ipsilateral Horner's syndrome, 3. Often follows head or neck trauma 4. May cause CRA or Ophthalmic Occlusion and finally Blindness. 5. Tenderness
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Asking the patient to show the location of his or her pain with a finger often is helpful. Trigeminal neuralgia is confined to one or more branches of the trigeminal nerve. Lancinating face pain triggered by facial or intraoral stimuli occurs with trigeminal neuralgia. (CBZ) Glossopharyngeal neuralgia typically is triggered by chewing, swallowing, or talking, although cutaneous trigger zones in and about the ear occasionally are present.
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Aura in Migraine Headache Intracranial Hemorrahges Carotid Dissection Neuralgias Basialr Type Migraine GCA
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Aura in Migraine Headache: Some patients with migraine have premonitory symptoms that precede a migraine headache by hours. These can include: 1. psychological changes, such as depression, euphoria, or irritability, or 2. somatic symptoms, such as constipation, diarrhea, abnormal hunger, fluid retention, or increased urination.
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focal cerebral symptoms associated with a migraine attack. most commonly last 20 to 30 minutes but can last 1 hour. Aura symptoms usually have a gradual onset and increase over minutes. usually precede the headache. But At other times, the aura may continue into the headache phase or arise during the headache phase. Visual symptoms are most common and may consist of either positive or negative phenomena or both. Other hemispheric symptoms, such as somatosensory disturbances (numbness and/or tingling) or language dysfunction, may occur with or without visual symptoms. If more than one symptom occurs (e.g., visual plus somatosensory), the onsets usually are staggered and not simultaneous.
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1. Positive symptoms 1. the slow spread of symptoms, 2. staggered onsets help
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Symptoms originating from the brainstem or both cerebral hemispheres simultaneously, such as: 1. vertigo, 2. dysarthria, 3. ataxia, 4. auditory symptoms, 5. diplopia, 6. bilateral visual symptoms in both eyes, 7. bilateral paresthesias, 8. decreased level of consciousness,
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The location of the pain is a poor predictor of the vascular territory involved. cortical infarction > deep cerebral hemisphere infarctions. either steady or throbbing and is rarely as explosive or as severe as the headache of subarachnoid hemorrhage. the pain is usually of at least moderate size, TIAs transient head pain in up to 40% of patients. carotid distribution ischemia frontotemporal head pain vertebrobasilar ischemia occipital headache.
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Female/ Obesity/Visual blur.) Drugs (/COPD/hirsutism/PCO Papilledema 6 th carnial nerve paresis No special focal neurological signs No other findings in routin lab No special finding in neuroimagining LP/Prednisone/Acetazolimide
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Most common feature: headache of an unknown cause. most common symptom headache (72%) The headache is most often throbbing + scalp tenderness. often generalized focal tenderness on the affected superficial temporal > occipital artery. Fisrt step: ESR
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New Headache Explosive headaches Worsening headaches Focal neurological sings Neck regidity Fever Trauma Inceasing pain with valsalva maneuver Confusion and decrease LOC AIDS Papilledema Old age Tenderness on the scalp Seizure Vomiting
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بیدار کردن بیمار از خواب سردردی که همیشه در یکطرف سر باشد تأثیر واضح تغییر پوسچر در تشدید سردرد.
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Dr. Boroumand
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Dizziness is a term patients use to describe a variety of symptoms including: 1. spinning or movement of the environment (vertigo), 2. lightheadedness, 3. presyncope, 4. Imbalance 5. visual distortion, 6. internal spinning, 7. nonspecific disorientation 8. anxiety
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sensation of spinning of the environment, indicates a lesion within the vestibular pathways, either peripheral or central
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Associated ear symptoms such as hearing loss and tinnitus can suggest a peripheral localization, to the inner ear or eighth nerve.
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Associated ear symptomes Positional dependency Onset pattern Focal neurological signs Risk factors
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Alertness Changes in severtiy by position changing Blood pressure (R/o for Ortho. Hypo.) Cranial Nerve Exam (at least 5,6,7,8) Ocular motor function Ataxia Coordination tests Sensation (specially vibration) Focal neurological signs.
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Peripheral pattern of nystagmus: 1. A peripheral pattern of spontaneous nystagmus is unidirectional; that is, the eyes beat only to one side. 2. It usually has a horizontal greater than torsional pattern 3. Suppression with visual fixation, 4. Increase in amplitude with gaze in the direction of the fast phase 5. Decrease with gaze in the direction opposite that of the fast phase.
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OKN and VOR-suppression Head thrust test Positing test Fistula test Otoscopy
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موفق باشید
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