MS2 Midterm PDF

MS2 Midterm Parkinson Syndrome- Referring to extrapyramidal disease, primary deficit is akinesia or hypokinesia. Bradykinesia- poverty of movements, reaction time delay and slow execution Rigidity- increased muscle tone(plastic type) w/o, significance loss of muscle power and increase in tendon re...

MS2 Midterm Parkinson Syndrome- Referring to extrapyramidal disease, primary deficit is akinesia or hypokinesia. Bradykinesia- poverty of movements, reaction time delay and slow execution Rigidity- increased muscle tone(plastic type) w/o, significance loss of muscle power and increase in tendon reflexes Resting Tremor- 3-5 per sec involving fingers, arm and chin *Suffer from postural imbalance Associated with Flexed Posture- head down on chest, shoulder rounded, arms and knee slight F Disequilibrium Festination- Series of quickening steps with propulsive/retropulsive character, Looking for COG Parkinsonism- Associated with drugs, a psychotic drug. identifiable cause is Drug. Dopamine is depleted, cause of other drug that compete with Dopamine *Symmetric *Tremor is uncommon *Hypokinesia tends to be symmetric *History of Drug ingestion Typical Drug cause Parkinsonism: Haloperidol *Sign occur after 3 mont of taking. Primary parkinson’s disease(Paralysis Agitants)- Adult-onset neurodegenerative disorder of extrapyramidal system. *Tremor at rest *Rigidity *Bradykinesia *Requires therapeutic response to levodopa *only neurodegenerative D long term treatment. *Cause is idiopathic *Asymmetric System Affected: Nervous, Musculoskeletal Genetics: Early onset 7x risk for having the disease Pathological findings- loss of pigmented cells in substantia nigra(pars compacta) and other nuclei in brainstem Substantia nigra- contain Dopamine 3 Black colored neuroanatomic structure: Retina, Substantia nigra, Hair. *Population of nigra cells fall from 425,000- 100,000 80% cell Die Diagnostic criteria Clinically possible if you have any one of: Rest tremor, Rigidity, Bradykinesia C Probable if you have 2: Rest T, Rigidity, Bradykinesia, Impaired postural Reflex One of 1st 3 displaying symmetry C Definite if you have 3- same as probable, any of 2 with one of 1st 3 displaying asymmetry Signs of PD(TRAP) Tremor- involuntary trembling of limbs( if happens in upper extremities called pill-rolling T) Rigidity- stiffness of muscle Akinesia- Lack of movements or slowness of initiating and maintaining movement Postural instability- F of the body, assoc. W difficulty in balance and disturbance in gait Cardinal Signs: *Tremor(4-8 hz) *Bradykinesia *Rigidity(Cog-wheeling w rest T) Other S/s: Speech poorly enunciated *Decreased blinking *Blepharospasm *upward gaze *Sebarate dermatitis *Constipation *Sexual Dysfunction * Depression (+) Dementia in 20% of pt. Tested by Folstein MMSE(minimal mental status exam.) *Gait disturbances- no arm swing, leaning posture, propulsion or retropulsion *Mask Facies- expression less face *Dysphagia *Daytime sleepiness increased Hoehn and Yahr Scale of Disability in PD Stage 1: uni/L, minimal functional impairment Stage 2: B/L w/o impairment of balance Stage 3: B/L, (+) instability, physically independent Stage 4: Severe Disability, can walk or stand w/o assist, but incapacitated Stage 5: Wheel chair bound or bedridden General measurement: Activity, Diet, Patient Education Therapy: Levodopa-carbidopa(Sinemet) Pathophysio- in PD decreased dopamine, increase ACH, target 2 things, elevate molecular concentration of dopamine and diminished effect of ACH Drugs Levodopa- Best drug for resolving parkinsonian symptoms, resolved by converting dopamine after crossing BBB Drug that reduce effect of ACH Diphenhydramine Trade name: Benadryl- use in cough remedy 75-200 MG Biperiden Akineton 6.0-8.0 Tyrosine(converted to dopa by tyrosine hydroxylase) Dopa(converted by dopa decarboxylase) → Dopamine *Dopamine cannot enter BBB, but levodopa can converted to dopa decarboxylase → Dopamine In periphery- Levodopa here is decarboxylated into dopamine. Carbidopa- block the decarboxylate of levodopa Levodopa → Dopamine w/o carbidopa cannot enter BBB, Need to decarboxylase by using carbidopa to enter BBB → once in CNS Carbidopa decarboxylase Levodopa → Dopamine Specific movement disorder Tremor- more or less involuntary and rhythmically oscillatory movement produce by contraction of reciprocally innervated muscle *Rhythmic quality distinguished tremor from other involuntary movement disorder *Involvement of antagonist and agonist muscle Characterizing Tremor: Rhythmicity, amplitude, frequency, relation to movement, postural set and relaxation Normal Tremor- Present in all contracting muscle groups, Persist in waking state and in phase of sleep. *Fine movement, ranges bet. 8-13 Hz *Average 10 Hz in adult and less in childhood Enhanced Physiologic Tremor- Same fast as physiologic tremor(10 Hz) but greater amplitude *Elicited when holding arm outstretched with fingers spread apart Seen in: Fright/ Anxiety, hyperthyroidism, hypercortisolism, hypoglycemia,Pheochromocytoma Intense physical exertion Abnormal Tremor- Affect group of muscle, distal part of limbs(Fingers and Hands) *Present only in waking state. *Rate is 4-7 Hz or half of physiologic tremor Essential familial tremor- AKA Familial hereditary tremor, Peak at >35 yrs old *Commonest type of tremor, 4-7 Hz frequency and worsen with age *It’s identified when attempting to maintain a static limb posture. Alcohol withdrawal tremor- Most prominent feature of alcohol withdrawal syndrome *Special type of action tremor related to enhanced physiologic T Parkinsonian rest T- Coarse, rhythmic with 3-5 Hz frequency *Burst of activities that alternate bet opposite muscle groups *Localized in 1 or both hands *Pill-rolling T- F/X or Abd/Add of fingers and hands Intention T(Ataxic T)- Occur in demanding phase of active performance *Action tremor(Kinetic T) *Always combined with cerebellar ataxia *Requires full expression of performance of an exacting, precise mov.(F-nose Test) Dystonic T- Do not overlooked are tremors are intermixed with dystonia. *Focal in neck, typically rotated *T is not rhythmic but jerky and intermittent Other T Primary orthostatic tremor- rare tremor isolated in the legs, occur during standing and cessation on walking. Hysterical T- Rare but manifestation of hysteria *Hysteria- exaggerated and uncontrollable Geniospasm- A strong episodic tremor disorder of chin and lower lip begin in childhood *Psychic stress and concentration are known to precipitate the movements Dystonia(Torsion spasm)- Manifested as posture in one or other extreme athetoid movement with predilection for muscle of trunk and limb *Heredodegenerative Disease Manifestation *Affect facial,oromandibular, tongue, cervical and hand muscle Chorea- Spasmodic, irregular movement of short duration involving fingers, hands, arms ,face *Syndenham’s chorea- neurological manifestation of rheumatic fever, anti-streptococcal antibodies cross react with neuronal tissue in BG *Hunington’s Chorea- emotional depression, irritability,apathy, slow progressive dementia, athetosis, rigidity and bradykinesia Athetosis- Irregular slow, sinuous movement involving hand and fingers *Also seen in biochemical disorder of genetic origin Ex. Aminoaciduria, PKU, lipidoses and leukodystrophies, Lesch nyhan syndrome and Wilson D. Clonus- refers to series of rhythmic, uniphasic(unidirectional contractions) and relaxations of group of muscle thus different in T which are diphasic(Bidirectional) and involve (B) agonist/anta *Epilepsia partialis continua- special type of clonus, series of rhythmic monophasic contraction W/o spreading Myoclonus- Arrhythmic shock like contraction of muscle groups, always asynchronous and asymmetric on 2 side of body. *Very brief last for 50-100 ms Polymyoclonus- widespread lightning-like a rhythmic contraction of muscle in many parts of the body Asterixis- Consist essentially of arrhythmic lapses of sustained posture. *Sustain muscular contraction allow gravity or inherent elasticity of muscle produce movement. Blepharospasm- involuntary blinking or spasm of orbicularis oculi muscle Myokymia- involuntary eyelid muscle contractions, involving lower eyelids *Excess caffeine, anxiety, fatigue, stress, lack of sleep drugs and alcohol Condition Associated with movement disorder Meige’s syndrome- AKA Brueghel syndrome, Forceful jaw opening associated with spasms of orbicularis oculi and other facial muscles Spasmodic torticollis- Rotation and retraction of head due to contraction of sternocleidomastoid, trapezius and other neck muscle Writer’s Cramp- Contraction of hand and forearm muscle during writing or performance of skilled motor acts. Syndrome De Gille Dela Tourette- multiple tics associated with sniffing, snorting, involuntary vocalization and compulsive obscenities *Caudate nucleus abnormalities Akathisia- state of motor restlessness *Complication of neuroleptic drugs *Tardive dyskinesia Tardive Dyskinesia- Consequence with long term therapy with neuroleptic drugs Phenothiazine and butyrophenones resulting super sensitive dopamine receptors *Involuntary movements of face, mouth and tongue(orofacial dyskinesia) Traumatic Brain Injury Demographics Males are likely to sustain TBI *Higher risk in males is true for all ages Etiology: Alcohol abuse is largest indirect cause of TBI *Fall are common in children and adult *MVA Pathophysiology Primary Injury- Occurs at moment of impact *Result of acceleration-deceleration injury *DAI, petechial hemorrhage *Parenchymal contusion, Cranial N injuries Diffuse Axonal Injury(DAI)- widespread stretching of axons, caused by rapid rotation of brain *Seen in severe injury *Initial loss of consciousness in TBI Primary TBI- Lesion are found where injury forces are greater(nearest surface of brain) *Often seen in interface of Gray and White matter *Petechial hemorrhage in MB, pons, Corpus C, Cerebellum white matter Secondary TBI- Physiologic and pathologic process triggered by primary initial injury, cause additional brain insult *One cause deterioration of patient *Include intracranial hemorrhage- epi,subdural and intracerebral *Vasogenic or cytogenetic brain edema *Oxidant injury, Hypoxia *Elevation in ICP((B) primary and secondary hematoma and edema) *Focal mass effect(hematoma) *Generalized mass effect(hydrocephalus) Closed head injury- Blunt non-penetrating, no direct connection by brain matter Whip splash injury- rapid acceleration-deceleration, cause atlanto-axial dislocation *Sudden application of physical force *Temporary LOC *Gross damage(Contusion,laceration, hemorrhage and swelling) *Shaken Baby syndrome Open head injury- direct communication in Brain parenchyma Cause by gunshot wound Result: Subdural and epidural hemorrhage Skull fracture and associated deficits Basal fracture → associated anosmia and apparent loss of taste sensation If Fracture near sella turcica → diabetes insipidus *Oculomotor nerve injury if → orbit injury *Affect ophthalmic and maxillary division of CN5 *Petrous fracture → CN8- disturbances in hearing Site of Brain Hemorrhage Intracerebral- occur inside brain, bleeding inside Subarachnoid- bleeding in subarachnoid painful kind, suffer from extreme headache “Worst headache of my life” Subarachnoid irritation due to blood corpuscles cause high pressure and result vomiting Subdural- Bleeding bet arachnoid and dura mater, blood accumulate resulting lucid interval Waking and wanging of consciousness Epidural- bleed bet. Dura mater and skull, slightly easy to access during surgery *Craniotomy Epidural Bleeding- common finding, occur 1% in cases but found 5 to 15% of cases of TBI Tear in middle meningeal artery *Happens in fracture of temporal bone 75% assoc. Temporal bone fracture Causing: Cardiorespiratory arrest 20% mortality rate Features: LOC, Lucid interval- LOC then regain and then loss again *50% gradual decreased in consciousness as ICP *NO lucid interval → poor prognosis Subdural Bleeding- Rapid accumulation of blood in subdural space Due to rapture of briding veins, transverse subdural space that bridge dural sinuses 50-80% mortality *Rapid LOC followed by rapid deterioration to coma and brainstem compression *Lucid interval *Suffer in uncal herniation and rostral caudal deterioration- Brain goes down into foramen magnum due to high pressure *Block in foramen luschka and magendie can cause increase ICP Treatment: neurosurgical evacuation of hematoma Chronic: Accumulation of blood or CSF, common in elderly and demented Alcoholics Acute: Slow accumulation of blood, develop increasing headache, drowsiness and progressive neurologic deterioration after recovery Cerebral concussion- not form of TBI,Close or blunt head injury with LOC *Reversible traumatic paralysis of nervous function *Accelerative and decelerative. *Mild Stuninng to LOC In severe: Brief bradycardia, Retrograde/anterograde amnesia- most reliable indicator of concussion. Cerebral Contusion-More wider in scope and extensive Result: Hemorrhage, secondary changes in contusion happens 12-72 hours after Coup-injury beneath point of impact, due to blow to front or side to side, common in frontal lobe Counter-coup- More extensive, contusion on side opposite site of impact *Due to blows in back of head or side *Brain bounces off Post-traumatic syndrome- AKA post-concussion syndrome Result: headache, dizziness, fainting and vertigo Read meaning of this term Head injury Assessment *Established ABC(airway breathing and circulation) of resuscitation *Evidence in skull laceration/bruising *Basal fracture sign: CSF rhinorrhea- coming out in nostril *Battle sign- bleeding over the mastoid *Use Glasgow scale *Pupil response *Limb weakness *Eye movement Management: Ensure airway and blood oxygenation Hematoma → evacuation Correct hypovolemia *Administer prophylactic antibiotics *Anticonvulsant *Diuretic(Mannitol)- reduce CSF pressure, Elevated head 30deg from the plane *Hyperventilate the lungs *Neuroprotective agents(Nimodipine- decreased ICF) GCS- higher score mortality is decreased Ex. Score of 4 → 49% mortality rate Pattern of recovery Sings of focal brain disease *Babinski sign - for hemiplegia *Aphasia *Brainstem disease * Stroke Sudden onset of focal neurologic deficit *Loss of motor control, altered sensation, cognitive or language impairment *Disequilibrium or coma *Caused by non-traumatic brain injury resulting from occlusion or rapture of cerebral BV *Aneurysm- dilated blood vessels *Exclude vascular lesion present as stroke(e.g. Seizure, syncope, TBI, brain tumor) CVD- Designated any abnormalities of brain resulting from a pathologic process of BV CVA- misnomers, confused vascular assessment Reversible ischemic neurologic deficit(RIND)- 1st kind of stroke, an infarct of cerebrum lasts longer than 24 hours. Transient ischemic attack(TIA)- Mini stroke, caused by change in Blood supply to a particular area of brain, resulting brief neurologic dysfunction *If symptoms persist it is categorized as stroke Amaurosis fugax- Ex. of TIA, defined as transient monocular blindness Due to episodic retinal ischemia Assoc. With ipsi/L carotid artery stenosis or embolism of retinal arteries resulting transient loss of vision in one eye Completed Stroke- Stroke syndrome with persisting neurological deficit, suggesting cerebral infarction Residual- when lasting for days, weeks or permanent with neurological difficulties remain. Stroke in evolution- Neurological deficits begin in focal then spread gradually. Reflecting involvement of more particular vascular territory *Monitoring neuro vital sign Making diagnosis 4 things to ask 1. Has patient had stroke?- not all acute focal neurological deficits are 2deg. To stroke Temporal may differentiate bet TIA, progressing, minor, severe or complete stroke 2. Where is the lesion?- Vascular territory: carotid Vs Vertebrobasilar 3. What is the lesion? Ischemia-most common type/infarction(w/or out hemorrhage) 4. What is pathogenesis? (MO stroke) Is it a stroke? Used to identify if stroke: Myriad differential diagnosis of stroke Other focal lesion: Tumor, abscesses, subdural hematoma, demyelination, focal encephalitis, herpes simplex can mimic stroke LMN: Bell’s palsy, plexopathies, mononeuropathy *Confusion, dementia and coma are presentations for stroke. Epidemiology- in PH second most common cause of Death Cause: High BP and Implicated substance abuse: methamphetamine or shabu Major type of Stroke Ischemic Stroke- 80% of all stroke type, result from focal ischemia leading to cerebral infarction *Mechanisms: Embolism, Small Vessel Thrombosis, hemodynamic from drop in local perfusion pressure. Global ischemia cause cardiac arrest or hypotension resulting “Diffuse encephalopathy” *Present in different size, anatomical loc and temporal pattern. Note: stroke comes from blood clot, coated by cholesterol called atherosclerotic clot Can occur independently or both. Carotid endarterectomy- procedure in secondary prevention of stroke Incision specific artery, extract plaque and repaired by stitches or put stent Hemorrhagic Stroke- Abrupt onset with focal neurological deficits, due to spontaneous bleeding.Non-traumatic *Include: intracerebral and subarachnoid bleeding *Subdural and extradural hemorrhage are not classified as strokes as they are trauma. Pathophysio- increased BP cause dilation of BV in Brain → weak BV → ruptured blood → Brain tissue → ICP increased Risk factors Non-modifiable- Age, heredity, Prior TIA or Stroke Modifiable- Hypertension- leading cause *Smoking *Oral contraceptive pills *Diabetes M. Other: CAD, PAD, Atrial Fibrillation, CHD, Sickle cell disease, Hypercholesterolemia Poor/salty diet, Obesity, Physical activity Salt- can increase inflow of water in intravascular space and can increase BP. Review of cerebral vasculature Carotid territory and Vertebrobasilar territory found in inf aspect of brain Direct connection in cardiopulmonary function and cerebral circulation Major Cerebral arteries: Carotid, Vascular, Vertebrobasilar artery. Note: Circle of willis- collateral circulation in brain- it mean when R side is block, mild damage occur but if both side can lead to: Diffuse Global ischemia Circle of willis-possess vessels which direct blood to different region in Brain, bounded by ICA, MCA, Basilar inferior, ACA, Ex/In Carotid Artery. Vascular territories Vertebro-basilar Territory Basilar artery- composed of penetrating arteries and composed AICA, PICA Sup cerebellar A.- supply upper portion of cerebellum, pons, internal auditory A. Carotid artery- give off ICA → Ophthalmic A(Big branch gives off retinal A. which is affected in amaurosis fugax) Ant Communicating artery and Ant choroidal Cortical Supply: Coming from Vertebro-basilar and Carotid A. MCA → Lateral, ACA → Ant frontal lobe, PCA → occipital lobe, choroid plexus, 3rd L vent lower surface of temporal lobe Stroke pathophysiology Ischemic stroke: subdivided base in occlusion Thrombosis- due to atherosclerotic plaque *Involves the common carotid and vertebrobasilar Embolism- occlusion is not stationary but mobile. Blood came from LV pump by weak heart after AMI(acute myocardial infarction) *Emboli of cardiac origin can cause *Atrial fibrillation- poor atrial mobility and stasis Lacunar infarct- a small stroke, < 1.5 cm or less Loc: subcortical region of BG, internal capsule, pons, cerebellum. Hemorrhagic stroke- caused by rapture dilated BV Intracerebral hemorrhage- rupture of deep perforating A. *Mostly in putamen and cerebral white matter *Special name to dilated BV- Charcot bouchard aneurysm Subarachnoid hemorrhage- bleeding within dural space and fills basal cisterns *Due to rupture of saccular aneurysm or Anterior-venous malformation(AVM) AVM- Abnormalities that deoxygenated and oxygenated Blood mix, due to artery and vein connection Types of aneurysm Saccular, Fusiform, Ruptured. Cerebral Angiogram- a technology can depict aneurysm. Anatomic Basis of Stroke Syndrome: Motor control/strength/ coordination/ balance. Spasticity, Sensation, Aphasia, Apraxia, Neglect syndrome, Dysphagia, Inhibited B&B Clinical Stroke Syndrome MCA Syndrome- mainsten, upper/lower division ACA/PCA/Vertebro-Basilar A.- All syndrome MCA Stroke Main Stem: if affected will cause following Contra/L Hemiplegia, hemianesthesia, hemianopia, head/eye turning toward lesion, Dysphagia, inhibited neurogenic bladders. Dominant Hemisphere: Global Aphasia, Apraxia Non: Aprosody/effective agnosia, Visuospatial deficit, neglect syndrome Upper Division: Note leg is spared than the hand and face will have S/s contra L Same as Main stem but leg is spared. Lower Division: More seen as ocular finding, cause contraL homonymous hemianopia Lesion in Optic nerve only: all of one eye is block therefore legally blind If optic chiasm- Half Visual Field of L eye L visual field and R eye R visual field If Optic Tract- Cause L visual field block and Left visual field block in Right eye- called ContraL homonymous hemianopia Dominant Hemi: Wernicke aphasia Non: Affective agnosia ACA Stroke- Contralateral hemiplegia(Spared hand), hemianesthesia Head or eye turning lesion, Grasp-reflex, paratonia, disconnection apraxia, akinetic mutism(Abulia) PCA- More visual pathway are affected Hence Hemisensory deficit, Visual impairment/agnosia, Prosopagnosia, alexia with agraphia Memory deficits. Horner syndrome- Triad of: Miosis, ptosis, anhidrosis Management for Stroke: Golden period for management to reduce neural impairment Maintain normal cerebral autoregulation *Cerebral perfusion rate 50 ml/100g tissue Acute ischemic S.- Treatment given is: intravenous recombinant tissue plasminogen activator(rt-PA)- function to lies blood clot a thrombolytic agent Heparin- to arrest stroke progression EMM(Emergency Medical Management) *Monitor ABC. *Watch for Cerebral edema, Hydrocephalus *Correct BP gradually *Correct hyperglycemia due to acute physiologic stress. Hemorrhagic stroke- to arrest the bleeding Coiling/clipping of aneurysm To Arrest hydrocephalus- a procedure occur called Craniotomy/Burr hole procedure Endovascular coiling- inserted mesh wire and a coil, will prevent dilated BV by rupturing Aneurysmal clipping- arrest bleeding immediately. Stroke prevention: reducing incidence of 1st time stroke Aspirin- avoid blood from clotting 160-300 ml per day Dipyridamole/ clopidogrel *Anticoagulation/plately therapy in atrial fibrillation Secondary prevention- Carotid Endarterectomy-relieving stenosis Diagnostic evaluation ,(Cranial MRI)- can locate the extend brain injury and detect other abnormalities CT, UTZ Rehab consideration Neurospasticity- Daily stretching, static resting splints for hand/ankles Botulinum toxic injection Sensori-motor control- Constraint induce movement therapy Body-weight supported treadmill training(BWSTT) When is the best time to rehabilitate pt?- When BP and VS is stabilize Treatment for Aphasia- Language oriented T. Direct stimulus response T. Visual action T. Oral reading for aphasia, conversational coaching Swallowing and nutrition- learning new swallowing maneuvers Percutaneous endoscopic gastrostomy tube- insert direct to stomach. Shoulder pain B&B Control- B&B Training, laxatives Psychosocial consideration For DVT- wear anti-embolic stocking cause compression in BV avoid clotting SCI Lec Main Syndrome *Transverse myelopathy- a complete sensorimotor myelopathy, involves ascending and descending tracts *Combined painful radicular and transverse cord syndrome. *Brown-sequard syndrome- AKA hemicord syndrome *Ventral cord syndrome- involve anterior colum, sparing post. Column *High-cervical foramen magnum syndrome. *Central cord or syringomyelic syndrome * Conus medullaris/ Cauda Equina syndrome SCI- one cause myelopathy or damage to white matter or myelinated fiber tracts that carry signal to and from brain. *Also damage gray matter in central part of spine, causing segmental loss of interneurons and motor neurons *Not excluding the destruction of dorsal root ganglia Epidemiology Highest bet. 16-30, 50% injuries occur. *Males present 81% and 89% of sports-related Both genders- auto accidents, falls and gunshots are 3 leading causes Males- diving accidents ranked 4th, followed by motorcycle accidents Females- Medical/surgical complications ranking 4th, followed by diving Auto accidents- leading cause of SCI in USA for people age 65 Falls- leading cause among 65 and older Sports and recreation-related- Affect under 29 yrs old Why diving can cause SCI- Diving and rising in surface, can cause molecular nitrogen to bubble up and cause embolism of BV in SC *Mechanical injury- due to abnormal flexion during a dive, decompression sickness Etiology Trauma, Tumor(Breast cancer,Meningiomas,)Ischemia(Occlusion of SC BV) *Developmental dis.-spina bifida, meningomyelocele *Neurodegenerative D- Friedrich ataxia *Demyelinative D- MS *Transverse myelitis *Vascular malformation- AVM, Dural arteriovenous fistula- dura mater has abnormal opening in SC, *Spinal hemangioma, Cavernous angioma, Aneurysm Sequelae of SCI- SC is irreversible, injury can result permanent damage Tissue disruption: Primary cell death, breaking axons → SCI show progressive tissue loss → Central hemorrhage necrosis develops 2-3 hours → White matter BF falls by 50% → metabolism is compromised with high lactic acid levels Apoptosis- Neuronal apoptosis peaks at 48 hours, after injury in gray matter *Oligodendroglial apoptosis peaks at 10-14 days after injury in degenerating white matter. Severed corticospinal tracts axons fail to regenerate- principle of absence of regeneration Stages of SCI Stage of Spinal Shock- Sensation and motor power localized below height of lesion are lost Ex. L5 gunshot wound below are lost all sensorimotor *Stage last for 2-3 weeks in humans, hours to days in lower animals due to lesser degree of encephalitis Stage of recovery- just only typical restoration of patter injury of nerve, partially recover and return of segmental reflex produce paraplegia in flexion Stage of reflex failure- pt. Reflexes back to normal, however giveaway to complete degeneration of nerve cells Review of normal SC anatomy *About 18 inch long *From base of brain to near waist *Bundle of Nerve fibers that make up SC contain UMN *SC nerve that branch off SC contain LMN Division- Four section C(1-7), T(1-12), L(1-5), S(1-5) Vertebrae Classification of SCI ASIA- defined an international classification based on neurological levels, touch and pinprick sensation test in each dermatome, and strength of key muscle Ex. Shoulder Shrug(C4), Elbow F(C5), West Ex(C6), Elbow Ex(C7), Hip F(L2) Traumatic SCI is classified into 5 types A- indicated complete SC injury no motor or sensory function is preserved in sacral Seg S4-S5 S4-S5 is the lower segmental, loss of sensory and motor function indicate complete. *Rectal Exam Complete SCI- cause all motor and sensory function below injury 50% are complete (B) side of body are equally affected. Commonly loss of function is caused by contusion. Key muscle to test in ASIA C5(Elbow F) C6(Wrist Ex), C7(Elbow Ex.) C8(Finger F)-T1(Finger abductors) L2(Hip F), L3(Knee Ex) L4(Ankle dorsiF) L5( Long toe ex) S1(ankle plantar F) B- indicated incomplete SCI which sensory but not motor function is preserved Sensation intact below neurological level *Typically a transient phase if person recovers any motor function below neurological level, become a motor incomplete C- Incomplete, motor function is preserved below neurological level and half of key muscle have a muscle grade of less than 3 D- incomplete, where motor function preserved and half of key muscle have muscle grade of 3 or more. E- Indicate is normal, Note that it is possible to have SCI and neurological deficit w completely normal motor and sensory scores. Reason why E is still positive in SCI 1. Error in examination, failure of physician to identify the S/M level 2. Test are premature after injury. Incomplete SCI Some function remains below primary level of injury, An incomplete SCI often falls into several patters. Anterior Cord Synd.- Result from injury to anterior column, causing weakness and loss of pain and thermal sensation below level of injury *Motor are disrupted *Preserve proprioception Cause:infarction in ant ⅔ of cord Clinical presentation: Flaccid paralysis below level of lesion Dissociated sensory loss: loss of pain/temp below LOL *Intact proprioception and vibration *Associated with: Atherosclerosis, hypotension, dissecting aneurysm Central Cord Syndrome(Syringomyelia)- Associated with greater loss of upper limb function *Result from trauma *Congenital syringomyelia *Damage to L Nerve Fiber carry info direct to Brain-SC Clinical Result: Paralysis and loss of fine control movements in arms and hands *Sensory loss below site of SCI *Loss of Bladder control *loss of pain/temp in cape like Horner’s syndrome- ptosis, myosis, U/L anhidrosis(if T lesion) *Segmental paresis w/LMN sign *Sacral Sparing Brown-sequard syndrome- Occur when injury to one side of SC, causing weakness and loss of proprioception on side of injury. Loss of pain/thermal in other side resulting Ipsi/L post. Column sensation loss, pain/thermal is contra/L Clinical Ipsi/L finding below LOL- UMN signs, loss of proprioception/vibration Ipsi/L findings at LOL- paresthesias and radicular pain(if R affected signs are within) Contra/L findings- Loss of pain/temp Tabes dorsalis- Injury in post. Column of SC, usually cause by Syphilis Degeneration of posterior column Clinical:Resulting loss of touch and proprioception sensation *Develops 10-20 yrs after Syphilis *Post roots also affected Triad: Lighting pains, Ataxia, Bladder disturbance Signs: Argyll-Robertson pupil- pupil will react to accommodation, but not to light Loss of proprioception(Sensory ataxia), Areflexia Conus medullaris syndrome- injury to the tip of SC, Loc at L1 Cauda Equina- Injury to spinal roots below L1. Cause lower urinary tract symptoms Spinal concussion- Can be complete or incomplete *Football players are susceptible Clinical manifestation: Numbness, tingling, electric shock-like sensation, Burning Ligamentous tears may be present Penetrating SCI- Common is gunshot wounds, require neurosurgical decompression *immobilized with a collar or brace if C region is affected Symptoms of SCI Extreme pain or pressure in neck, head or back Tingling or loss of sensation *Partial or complete loss of control any part of body *Urinary or Bowel incontinence *Balance/ walking difficulty *Band-like sense in T *Impaired breathing(if C4 C5 affected) *Lumps on head or spine Complication of SCI Pneumonia, Decubitus ulcers: Most common *GI Hemorrhage *Thrombophlebitis *Pulmonary embolism *Arrhythmia *Wound infection *AMI Surgical advances: Decompression and stabilization of spine using Fusion Rod Laminectomy- removal of vertebrae lamina reducing compression in DRG Congenital Cord Syndrome I-Neurologic disorder associated with craniospinal deformities *Enlarged head *Craniosynostosis- Abnormal fusion of fibrous suture *Dist. Of neuronal formation & migration *Microcephaly *Comb. Of cerebral/cranial *Rachischisis- neural tube defect *Chromosomal Abnormalities. II-Phakomatoses: inherited dis affect skin and NS III- Restricted Dev. abnormalities of NS IV-Congenital abnormalities of motor function (CP) V- Prenatal and Perinatal infection VI- Epilepsies of infancy VII-Mental Retardation Dysraphism and Rachischisis -Disorder of fusion of dorsal midline structure in primitive neural tube -Process takes place during first 3 week of postconceptual life. Encephalocoele- Eventration of brain tissue and its covering through an unfused midline defect in skull Mengio Encephalocoele- Connected with rest of brain through small opening Dandy-walker syndrome- Failure of development of midline portion of cerebellum *Dilated 4th ventricle *Abnormalities closure of vertebral arches Spina bifida occulta- premature development, cord remains inside canal and no external sac. Subcutaneous lipoma may mark in skin on site of lesion Congenital Birth Defects: Spina bifida, Hydrocephalus and Arnold-Chiari malformation Meningocele- Protrusion of Dura and Arachnoid mater only *Defect in vertebral laminae *Common in lumbosacral region *Forming cystic swelling *Cord remains in canal Meningomyelocele- 10x frequent as meningocele *Cord more often the cauda equina *Extruded and closely applied to fundus of cystic swelling Spinal Dysraphism- Myeloschisis, Varies widely from one locale to another *Occur in second child if previous child has been affected * 1 per 1000 to 40- 50 per 1000 Motor neuron disease of infancy and childhood Spinal muscular atrophy(MSA)- progressive weakness & atrophy *Degeneration of anterior horn cells(LMN) *No UMN sign *recessive Survival motor neuron(SMN) gene on chromosome 5 *95% have deletion that prevent expression Werdnig-Hoffman: Floppy infant, Anterior horn cell degeneration of SC 39) not prolonged fever 6 months- 6 years common in boys Cause: No known, but may be hypersensitive hypothalamus or genetic Types of BFS Simple FS- Most common, short duration no focal features duration is less than 30 sec Generalized FS- CFS, increased risk of death Clinical diagnosis- Body become stiff and arms/legs begin twitching LOC *Irregular breathing *Vomit *Incontinent Treatment: Control fever *Clonazepam Peripheral Nerve Injury Nerve cell composed: soma and axon arranged in systematic Spinal nerve root → from Union of Ant/Post root ganglion Radiculopathy- compression of Spinal nerve SN- incase in fibro collagenous connective tissue Disease can affect it is: Lupus erythematosus, sarcoidosis, amyloidosis Epineurium- cover entire nerve fascicle Perineurium- cover entire bundle Endoneurium- cover individual nerve Symptomatology of PND *Impairment of motor function if anterior Polyneuropathies- Marked by symmetric distribution of weakness DAI affects feet, legs early and severely than forearms and hands. *Due to long axon traversing to legs rather than forearms S/s: if chronic motor, muscle atrophy and absent reflexes If sensory, paresthesias in addition to sensory loss *Autonomic dysfunction *PNI- is LMNL Mononeuropathy- is usually proximal and upper ex. Fiber size selectivity- Large: Motor weakness, loss of joint position, vibration and touch/pressure Small: Pain and temp. Loss, autonomic dysfunction(C fiber) *Relationship to systemic illness(MA,RA) Test to rule in Neuropathy- NCV or EMG with quantitative sensitivity testing Sensory phenomena Negative P- Difficult to discriminate texture, loss of pain and temp joint position perception *Unsteady gait Positive P- Diseases of L myelinated fiber, producing paresthesias:”pins and needle” sensation with peripheral distal distribution Including: Dysesthesia- Painful when touching *Hyperalgesia- Threshold to pain appears lowered *Hyperpathia- Pain threshold is elevated but once reached painful stimulus is excessively felt *Lightning pains- Sudden severe shooting pain *Causalgia spontaneous burning sensation. Sensory examination Light touch, 2-point discrimination and vibration sense- for L myelinated fiber Temp/Pain and joint position perception- for S myelinated fiber *Motor examination Acute- few days to 4 weeks Cause: Post infectious Guillain-Barre→ Motor, distal or proximal autonomic disturbance → Demyelination with perivascular lymphocytic infiltration *Diphtheria → Cranial N. mixed sensorimotor → Demyelinating, No inflammatory infiltration *Porphyria → Motor, autonomic disturbance → Axonal Subacute- develop over weeks Cause: Drug induce like INH(Isoniazid) for TB → mild sensory motor Dapsone for leprosy → Pure motor involvement both are axonal degeneration *Sensory loss either Negative or positive phenomena *Dimunation of reflex