Understanding Levels of Consciousness, Intracranial Pressure, and Seizures in Neurology

1. Chapter 61 Level of Concsiouness Headache Intercranial Pressure Seizure

2. Level of Conscoiuness • Can be any spot on a spectrum from normal to coma • Full Conscoiuness would be orineted x’s 4 • Person, place, time, and sitution • Coma • AkineticMutism • Vegetative State • Locked-in Syndrome

3. Level of Consciousness • PATHOPHYS • LOC is not a disease in an of itself but instead a symptom of another condition • Manifestations • Rememeber the GCS • Diagnostics • Full neurological assessment • Labs (cbc,cmp,NH3, LFT, Ca++, urine) • Test (MRI, EEG, CT)

4. Increased Intracranial Pressure • Normal level is 0-15 • Monro- Kellie Hypothesis • the sum of volumes of brain, CSF, and intracranial blood is constant (Morki, 2001) • If one expands or decreases then the other need to compensate Morki, B. (2001). The Monro-Kellie Hypothesis. Neurology. 56(12).

5. Pathophysiologyof ^ ICP • Commonly associated with head trauma but also seen with tumors, metabolic acidosis, edema and herniation. • Decreased blood flow • Cell death +/- ischemia causes system pressure rises • This can produce a slow bounding pulse with respiratory irregulatories

6. Pathophysiology • Cerebral Edema • Abnormal association of water and fluid in the intra and extra areas with an associated an increased volume of Hisse • Autoregulation occur as blood vessels constrict and diliate to keep the blood flow • Cerebral response to increase ICP • CPP= MAP-ICP • Normal CPP= 70-100 mmHg

7. Cerebral response to ICP • Steady perfusion continues with ICP <40 & SBP 50-150 • CPP<50 = irreversible neuro damage • If CPP=ICP No cerebral circulation

8. Ceberbral Response Cushing Response Cushing Triad Decreased Heart Rate Increased SBP Decreased Respiration • Widening pulse pressure • Increased SBP • Decreased heart rate • Considered a late sign but still may be treated

9. Clinical Manifestations • #1 sign of increased intercranail pressure is changes in LOC • Any sudden changes in the neuro status is significant • As ICP increases becomes stuporous, only reactioning to only loud painful stimulus

10. Posturing

11. Assessment of ICP • CT, SPECT, cerebral angiography • LP’s are contrindicated if the person is believed to have increased intracrainal pressure

12. Seizure Disorder Abnormal motor sensory autonomic, or orpysch disorder Due to excessive discharge of neurons Can have 2 classifications partial(simple/complex) general SEE BOX ON PAGE 1881

13. Epilepsies • Known as a reoccuring seizure • May be primary or secondary • Pathophysiology • Neuron discharge by electrochemical energy to perfer a task • When they are supossed to stop they continue to firing the impluse which lead to a seizure

14. Eplisies Clinincal Manifestations Assess & Diagnosis Detailed Health History Family History Physical and Neuro Status MRI/EEG- localizes the area better; they may also need to do telemtry EEG In the elderly epilpsey can present as an CVA Status Epilipticus • Depends on what neurons are firing • Could be a small twitch that doesn’t stop or could include decrease level of consciousness

15. Headache • Most common neuro problem • May be primary but for unknown reasons • 3 types • Migrane • Tension • Cluster • Arteritis

16. Pathophysiology • S&S of a migrane result from dysfunction of the brain stem pathways that modulate sensory input • Caused usually by vasodilation • May have many different triggers • Tension-usually associated with stress • Cluster-????? • Arteritis-migrane response when complex are deposits in the blood vessels walls

17. Migranemanifestions Migrane Manifestation Tension Constant steady pressure feeling state @ temple, front of head, or back of neck Arteritis Very general start malise, fatigue, wt loss, fever, may swollen tender • Prodrome • Aura • Headache • Recovery Cluster • Unliateral small and frequent • May 1-8 x’s/day • Last 15 min- 3hr

18. Assess & Diagnostics • Detailed history • Must be very detailed • Need to determine if the cause is something