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 – Akinetic Mutism – 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,NH 3, 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. Pathophysiology of ^ 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 Widening pulse pressure Increased SBP Decreased heart rate Considered a late sign but still may be treated Cushing Triad Decreased Heart Rate Increased SBP Decreased Respiration

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 or pysch 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 Depends on what neurons are firing Could be a small twitch that doesn’t stop or could include decrease level of consciousness 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

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. Migrane manifestions Migrane Manifestation Prodrome Aura Headache Recovery Cluster Unliateral small and frequent May 1-8 x’s/day Last 15 min- 3hr 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

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