Pathophysiology ALS {Ans: Most are sporadic and not familial Increased glutamate in CNS Mitochondria malfunction Impaired axon/transport Genetic fluence Oxidative stress}Exam: CVA {Ans: ABCD score ABC's Neurologic exam ICH: aging, SBP >220, severe HA,,, LOC change, symptom progression over minutes to hours NIH scale}CVA {Ans: Ischemic: interruption of blood flow Hemorrhagic: rupture of artery that's been weakened by hypertension Modifiable RF: HTN, DM, smoking, hyper, lipidemia, obesity, poor diet, physical inactivity 5th leading cause of death Blacks}CP/exam {Ans: Carotid: ipsilateral eye/contralateral body Transient painless, loss of vision Weakness/numbness of contralateral, face or limbs Language difficulties Cognitive changes Vertebrobasilar: vertigo, N/V, nystagmus, diplopia, disconjugate, gaze, CN deficit SAH: thunderclap headache, N/V, LOC, atypical HA days two weeks before Hypertensive ICH: no prodrome, happens while patient is active, elevated BP, Immediate into stupor/coma, hemiplegia, then death Occurs over 5 to 30 minutes Advanced cases, paralysis, aphasia, stupor coma, deep/irregular respiration dilated/fixed pupils, decerebrate rigidity A/P circulation: hemiparesis, hemi, sensory loss, visual field deficit, ataxia, dysarthria, reflex asymmetry, Babinsky}Diagnostics ALS {Ans: Widespread UMN/LMN signs in absence of electrophysiologic/pathologic signs Absence of Neuro imaging evidence Diagnosis of exclusion No laboratory/biochemical markers Order EMG/nerve conduction studies for suspected ALS MRI: