Neurological Disease PDF
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Misurata University
Dr. Abdulraouf Abdullatif
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This document provides an overview of neurological diseases, covering the central nervous system (CNS) and peripheral nervous system (PNS), including the brain, brain stem, and cerebellum. It also details the functions of these structures and components, such as the frontal, parietal, temporal, and occipital lobes, and the brain stem.
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By Dr : Abdulraouf Abdullatif Neurological disease Nervous system is composed of : Central nervous system Peripheral nervous system CNS...
By Dr : Abdulraouf Abdullatif Neurological disease Nervous system is composed of : Central nervous system Peripheral nervous system CNS PNS 1- brain Spinal cord 2- brain stem segments (31) 3- cerebellum Central nervous system CNS: 1- brain: is composed of 2 cerebral hemispheres ( RT & LT ) , each cerebral hemisphere is composed of many lobes which contain many centers. & tracts ( moter & sensory) *Frontal: Personality - Emotional control - Social behavior - Contralateral motor control - Micturition centers * Parietal: Language( speech) – (Calculation, Visual Spatial, Constructional skills memory centers) & optic tract * Temporal: Auditory - Verbal memory - Smell centers * Occipital: Visual centers The brain stem: is composed of 3 parts: 1- mid brain 2- pons 3- medulla oblongata Function: 1-contains all the sensory and motor pathways 2- nuclei of the cranial nerves ( all except 1 & 2) 3- some centers( respiratory centers, conscious centers, sy mpatatic chain) > wernick area > responsible of reading and writing 144) Cortical Skills Astereognosis is used to describe both the inability to discriminate shape and size by touch and the inability to long term recognize objects by touch. memory agraphesthesia, involves the inability to recognize visual cortex letters or numbers drawn on the hand. % 9944 = ente - ~ - genu of internal capsule descending tract of motor sensory tract وهيا راكبه cranial nerves 7, 12 Internal capsular lesion: 1- contralateral hemiplegia or paresis 2- contralateral hemi sensory loss of body 3- CN impairment 7,12 4-auditory + vision impairment The Internal Capsule:- This is a compact bundle of fibres through which the large collections of fibres pass, including: 1- The thalamocortical & corticothalamic fibres 2- corticopontine, 3- corticobulbar. 4- corticospinal fibres. S. cord end at level of Le 3 - 4 as condensation > Conus 5. 7 , 6 , 8 medularis · epiconus -J 9. 10 , 11. 12 CSF > under level 11 and La · - white matter > act as Cushing lower order neuron reflex - in grey matter Sudden reflex not need to go to brain like put hand on fire · - Sphincter.....? start from motor Alte > Spinal Segment > Dn > nm( sensory-sensory system > DHC motor and sensory > Bundle > PnS By Dr : Abdulraouf Abdullatif Cerebullum: which is composed of 1- 2 lateral hemispheres 2- vermis 3- folcculonoduler lobe Function: “coordination”(balance) of peripheral& axial of body & balance of eye & ear function The spinal cord: composed of 31 segments which ends at level of L1 by cones medullaris & coda equine, spinal cord has 2 components : 1- Gray matter contains: * 2 anterior horn cells ( motor nuclei ) * 2 posterior horn cells ( sensory nuclei) * collections of cells which are responsible for lower-order reflexes 2- White matter contains: * afferent and efferent fibres of moter & 2- Whi te ma tter 1- Gray ma tter sensory tracts * stabilizes the spinal cord PNS: ant.horn cell of spinal cord segment --- peripheral spinal nerve --- neuro muscular junction --- mscle Functional neurology : Lower ordered reflex’s 1- motor system 2- sensory system Cerebellum 3- cranial nerves By Dr : Abdulraouf Abdullatif The motor system: is composed of Pyramidal Tract Extra - Pyramidal Tract (Voluntary movements) (Involuntary movements) How should I move If there is CST CBT abnormal movement Cortico spinal tract Cortico bulber tract not weakens If there is weakness Function of Basal Spinal nerves Cranial nerves ganglion CST: (UMN) course: A programme of movement formulated by the pre-motor cortex is converted into a series of signals in the motor cortex. This passes through the Posterior limb of internal capsule until the anterior 2/3 where it prices into brain stem - mid brain – pons - medulla & oblongata where it decussates in the lower 1/3 and descends into lateral columns of the spinal cord & end by synapsing with the anterior horn cells of the spinal cord grey matter. from which form the peripheral spinal nerves 'lower motor neurons' N.B Muscle reflex arch UMN (-) LMN (+) In the most inferior (caudal) part of the medulla, the tract divides into two: The fibres within the lateral corticospinal tract decussate (cross over to the other side of the CNS). They then descend into the spinal cord, terminating in the ventral horn (at all segmental levels). From the ventral horn, the lower motor neurones go on to supply the muscles of the body. The anterior corticospinal tract remains ipsilateral, descending into the spinal cord. They then decussate and terminate in the ventral horn of the cervical and upper thoracic segmental levels. 80 % >decusation , 20 % same side I ipsilateral no significant clinically UMHL > 1 - Cortical 2- capsular contralateral 3- brain stem ↑ Spinal cord ipsilateral · reflexes LMHL > 3- AHC > inhibit 2- Dh Segment umn Lin > stimulate 3- n - nmj 5-muscle capsular stroke Its haemorrhagic bleeds Such an event could cause a lesion of the descending tracts. By Dr : Abdulraouf Abdullatif Motor system lesions: UMNL LMNL Inspection: Ms. Bulk = normal Ms. Bulk = marked atrophy ( but if mild a trophy due to disuse) NO fasciculation’s + ve fasciculation’s Tone Hypertonia = spasticity Hypotonia = flaccidity Clasp knife spasticity power Decreased decreased reflexes Abdominal: -ve Abdominal: -ve Cremasteric: -ve Cremasteric: -ve Anal: -ve Anal: -ve Planter reflex: babenski +ve Planter reflex: -ve Ankle clones: +ve Ankle clones:-ve Deep reflex: hyper reflexia Deep reflex: hypo reflexia DD: 1- CVA 1- ANC = Poliomylites 2- MS 2- PSN = GBS 3- MND 3- NMG = MG 4- Space occupying lesion 4- Ms. = congenital ms disease 5- spinal cord lesion motor defect localization brain:- Cortical defect internal capsule brain stem. contralateral 2 hemi/Paresis. Contralateral 1 hemi/Paresis 1 - / ↓ / or plasia or plasia 2- focal neurological defect 2 sensory defect C - ch defect ipsilateral 3 - 7 12. Spinal cord defect : - C1-C5 : - above brachial plexus hemi cut > hemiparesis or plagia both UL , IL 1) spastic because of UMHLi complete cut Death because of brachial plexus supply respiratory muscle CS-Ts : above Brachial Plexus hemi cut cut the central nerve system and peripheral nerve above ty > lead to hemi weakness > uh > flaccid 1) ImnL LL > Spastic PutukLi complete , cut same but qudri weakness rL > flaccid LL > spastic The brachial plexus is formed by the anterior primary rami of C5 through T1 below TJ above bellow the brachial plexus Lambosacral hemi cut > Mokoparresis only one leg spastic lesion Duma Li , complete cut> both leg spastic > Lambasacral : ↳ mean Peripheral nerve Segment itself hemi cat one leg weakness flaccid ((mk) complete > cut both leg > paraparesis flaccid Is By Dr : Abdulraouf Abdullatif Cerebellum clinical lesion : Face 1- head nodding & titubation 2- dysarteria = Staccato ,scanning, explosive speech 3- horizontal nastugmus Upper limb Lower limb 1- finger nose test = 1-heel shin test = impaired intention tremor & dysmetria 2- Gait = ataxic gait 2- rapid alternating movements = 3- Romberg sing = +ve dysdiadokinesia 3- rebound test = over shooting Cerebellum lesion : Ataxia it’s in the same side of lesion By Dr : Abdulraouf Abdullatif The sensory system: Pathway: Posterior(dorsal) column Spino talamic (anterior lateral) sensory tract sensory tract By Dr : Abdulraouf Abdullatif Sensory pathway of face: Sensory dermatomes of body: By Dr : Abdulraouf Abdullatif Localization of lesion: Cerebral hemisphere Brain stem SPINAL CORD Hemi cut C1 above C5 Complete cut above C5 Hemi cut C5 C5-T1 Brachial plexus Spinal cord lesion Complete cut C5 – T1 If Hemi cut : ipsilateral PCS lost & Hemi cut T1 contralateral STT lost (brown squard T1 - L1 syndrome) below site of lesion Complete cut T1 – L1 L1 If complete cut : complete sensory lose Hemi cut below site of lesion Below L1 Lumber plexus Complete cut Below L1 · deep mean In tendon , ms · sensation of face from trigeminal nerve The dorsal column-medial lemniscal pathway (DCML) carries the sensory modalities of fine touch (tactile sensation), vibration and proprioception. except fine touch anterior Limb of internal Capsule decusation X * trigeminal It's brunches · decussation at upper border of midbrain By Dr : Abdulraouf Abdullatif Site of lesion: Motor system Sensory system Cerebral Contra lateral hemi (plagia or Contra lateral sensory loss of hemisphere paresis ) Face & Body UMNL IN UL & LL Brain stem Contra lateral hemi (plagia or Ipsilateral sensory loss of paresis ) face UMNL IN UL & LL contra lateral sensory loss of body Hemi cut Ipsilateral hemi (plagia or above C5 paresis ) UMNL IN UL & LL Face : normal sensory Complete cut DEAD If Hemi cut : ipsilateral PCS above C5 lost & contralateral STT lost Hemi cut Ipsilateral hemi (plagia or C5-T1 paresis ) (brown squard syndrome) (LMNL in UL) & (UMNL in LL) below site of lesion Complete cut Quadri (plagia or paresis ) If complete cut : complete C5 – T1 (LMNL in UL) & (UMNL in LL) sensory lose below site of Hemi cut Ipsilateral mono (plagia or lesion T1 - L1 paresis ) (UMNL in LL) Complete cut Para (plagia or paresis ) T1 – L1 (UMNL in LL) Hemi cut Ipsilateral mono (plagia or Below L1 paresis ) (LMNL in LL) Complete cut Para (plagia or paresis ) Below L1 (LMNL in LL) By Dr : Abdulraouf Abdullatif Cerebro-vascular Accident. Anatomy: Brain is supplied by 2 main systems: 1/Carotid system: ICA ACA & MCA supply cerebral hemisphere. 2/Vertebral basilar system *Basilar A. *PCA Each artery supplies part of brain: 1/Anterior Cerebral Artery: supply frontal lobe (Personality - Emotional control - Social behavior Micturition centers - Contralateral motor control - & Sensory tracts). 2/Middle cerebral artery: supply Temporal & parietal lobe *Parietal: Language( speech) – (Calculation, Visual Spatial, Constructional skills memory centers) & optic tract *Temporal: Auditory - Verbal memory - Smell centers also motor and sensory tract. 3/Posterior carotid artery: visual centers. 4/Basilar artery: Brain stem (Cerebellum – all C.N except 1 & 2 - Res center Sympathetic nucleus – conscious center) N.B: 1/ Motor if affec ted contralateral hemi plegia/ paresis. 2/sensory if affected contra lateral hemi sensory loss 3/ *ACA L.L > U/L & face. *MCA U/L & face > L.Li mb. *PCA face & U/L > L.limb. By Dr : Abdulraouf Abdullatif Def of CVA: Acute neurological defect due to vascular cause. 1/ Ischemic CVA (85%): *EIDIMIOLOGY: *Embolism MCC ( heart= A.F) -3th commonst *Thrombosis. cause of death in *Hypotension. devolved countries. *Arteriosclerosis. *Vasculitis. Common -> in black. *Space occupying lesion. –Age>40. 2/Hemorrhagic CVA (15%) –Female > male. D/D of CVA: *Risk factors: 1/Hypoglycemia. 1/Hyper cholestrolemia. 2/Space occupying lesion. 2/uncontrolled HTN & D.M. 3/Encephalitis. 3/Obesity. 4/Epilepsy(Todd’s palsy). 4/smoking. 5/peripheral neuropathy. 5/lack of exercise. 6/Alcohol. Lasting 7/OCP. 24hr -Transient Ischemia Attack (TIA). -Stroke. *Acute Neurological defect due to *Acute focal neurological defect due to vascular cause lasting 24hr. *TIA: *Minor Stroke: *Progressive *Complete stroke: symptom > 24hr but stroke: Symptoms Rapid maximum -source of embolism is. without resolve worsen due to persistent neurological carotid artery affect significant defect. increase size of defect within few MCA & Retinal artery. infarction hours due to multiple –Any ptn with TIA do emboli. (Doppler-Duplex U/S). By examination: 1/Amuorosis fugues. 2/Auscultation (Carotid Bruit not always). The right vertebral artery. Superiorly, it converges with the left vertebral artery to form the basilar artery ① Continuation ICA IS MCA ACA · > supply frontal lobe The middle cerebral artery (MCA) - supply temporal lobe , partial lobe , part of brocks area , speech problem may due to MCA lesions ·. ICA < represent anterior circulation vertebral represent · artery posterior circulation ·- ACA - occlusion - frontal lobe defect hemiparesis> more in upper limb occipul Lobe MCA occlusion · , visual and memory defect asteriognosis , aacalculia , dysphasia F brain contralateral homonymous hemenopia Star branch of vertebral artery before enter foramen magnum > supply lateral side of brain stem DICA Chain Ch Cerebellum , Sympathetic , , tract-lateral spino thalamic sensory Ch , 5 , 9 , 10 11 , PICA because It's area It's common to be narrow very * - in obstructed Lateral and cause medullary syndrome ataxia , Horner Syndrome , Ch Lesion , contralateral sensory loss 1) Crude touch , pain , temperature superficial By Dr : Abdulraouf Abdullatif *C/P: -ACA occlusion. 1/contralateral hemiplegia or paresis. 2/contralateral hemisensory loss (L.L>UL & face). 3/Emotional changes. 4/Behavioral & personality changes. 5/ urine incontinence -MCA: 1/contralateral hemiparesis or plagia. 2/contralateral hemisensory loss (UL & face > LL). 3/auditory & smell disturbance. 4/aphasia: -if Broc’s area is affected ( broken speech). -if Wernichs area is affected (Wordy speech). 5/Impaired memory: especially visual spatual memory, calculation, constructional skills. 6/contralateral homony mous hemianopia. * if only PCA -PCA: Basilar occlusion (Brain stem infarction) - visual 1/Contralateral hemiparesis & hemiplegia. hallucination 2/Contralateral sensory loss of (UL > L.L) of body. only 3/Ipsilateral sensory of face Ptosis. 4/Ataxia (cerebellum lesion). Meiosis. 5/Cranial Nerve palsy (7,9,10,11,12). Anhydrases. 6/Visual hallucination & visual loss. Enophthalmus 7/Hornor syndrome. 8/Locked in syndrome (loss of consciousness, can move eyel id). 9/Respiratory failure type II. · motor defect is the same in upper and Lower By Dr : Abdulraouf Abdullatif *Inv: 1/To confirm Dx : acc to site -C.T: sensitive in detecting strokes due to (ACA & MCA) Occlusion aim to exclude hemorrhagic CVA, by distinguishing between infarction (Black) & Hemorrhagic (White), changes of infarction need 48hr to appear. But high Resolution C.T scan 12-36hrs. -MRI: sensitive in detecting strokes of the brain stem & cerebellum due to occlusion of basiler & PCA to exclude hemorrhagic CVA. 2/To detect the cause: a) LAB, -CBC Polycythemia & thrombocytosis. -WBC, ESR, & CRP due to clot or vasculitis & SLE. -Antinuclear Ab when suspect vasculitis due to SLE. -RBS. -Lipid profile. b) Imaging: chest X-ray for aspiration pneumonia. *ECG. *Doppler U/S of carotid artery. both after stabilization of Ptn *Complication: -Chest infection Most Common Cause of death. -DVT&Pul monary embolism due to immobilization & hyper coaguble state (2 ndcause of death). -UTI & Constipation b/c immobilization. -Epilepsy & dementia. -Depression. -Painful shoulder b/c of stagnation of B.V around shoulder joint. By Dr : Abdulraouf Abdullatif *Management of Stroke: Admit The Pts Primary survey A,B&C. A patent air way. B Breathing, give ptn 60% of O2for brain. C circulation, insert 2 large cannula send blood for Ix. Measure Bp if hypotension give Iv fluid (5% dextrose saline), if there is no C/I but don’t over hydration Cerebral edema. -NGT insertion for gastric lavage & prevent aspiration pneumonia. -Insertion urinary catheter. DO MRI or CT. *Hypo dense (Infarction) * Hyper Dense (White lesion) early stage no changes. 6hr -Neurosurgeon Consultant. *Thrombolytic given with a caution -Prevent further stroke. & only if no C/I. –Aspirin 75mg + Dipyrida mole 200mg. –Not given > 6hrs b/c need high dose -Control DM & Bp. thrombolytic, -Lipid lowering agent (sta tin or omega3). which lead to rupture Hemorrhagic –Control R.F. CVA. -Physiotherapy + Rehabilita tion decrease -Management of TIA: Complication 1/Aspi rin 75mg long life. 2/Rx the risk factors. Control Bp: transit HTN seen after stroke usually does not 3/Regular Duplex U/S of carotid vessels require Rx, but if Bp >230/100mmhg or end organ damage if >70% occlusion stent is required. ptn require gradually slowly in Bp 160/90. Anticoagulant is C/I. By Dr : Abdulraouf Abdullatif Hemorrhagic CVA: D/D: Sunstroke –- Subarachnoid He -- Hypoglycemia -- Drug addict Subarachnoid He Intra cranial He Causes: 1- Rupture of secular aneurism 1-Rupture of micro B.V 2- berry aneurism 2-Buchard Charcot B/c HTN. 3- A-V malformation (Idiopathic). CP: -vomiting. -vomiting. –blurred vision due to –blurred vision due to papilla edema papilla edema –irregular respiration. –irregular respiration. -Neck stiffness. -Neck stiffness. –coma –coma –occipital Headache –Frontal Headache Dx: CT OR MRI. CT OR MRI Lumber puncture Xanthocromia If there is no CT or MRI fundoscopy after 12hr (yellowish pinkish Papilledema. & CN VI (lateral rectus b/c has CSF) long intracranial root). Rx: -Bed Rest. -Bed Rest. -control Bp gradually. -control Bp gradually. -Dexamethasone & Mannitol. -Dexamethasone & Mannitol. -Urgent neurosurgery -Urgent neurosurgery -consultant call -consultant call By Dr : Abdulraouf Abdullatif Multiple Sclerosis D/D: 1- M.S 2- Vit B12 Def Def: Multiple neurological sclerosing defect separated by 3- Transverse Myelitis space & Time. 4- sub-acute sclerosing pan encephalitis. Causes: Demyelination. 1/T-lymphocyte mediated autoimmune response T cell after pass BBB Recognize a Myelin as FB this leads to secretion of inflammatory mediators CD4 & IL & TNF damage, Gliosis. Female > Male ( 20-40yrs). +ve F/H. HLA Dr2. Ab in CSF oligoclonal band IgG 80% - one heavy chain. 2/ Post Viral infection (Measles), Measles Ag-Ab 2ry Ab against Measles Ab in CSF. 3/Environmental: Hot Climate and improve in cold climate C/P exacerbation during hot bath.( uttofs sy mptom SPACE TIME *-Relapsing & Remission(80%). تمشي وتجي والترجع للطبيعي -2ry progressive مع الوقتcontinuously & constant. -1ry progressive (steady progressive). -progressive Relapsing. سريعة هلب 1/Optic Nerve: (Most common site): a/ Painful unilateral optic neuritis, start unilateral then bilateral. b/ Diplopia: due to optic neuritis decreasing in propagation of single image less than other eye. By Dr : Abdulraouf Abdullatif c/ Impaired colure vision (Rods & Cons). d/ Nystagmus: due to diplopia. 2/ Brain: a/ Motor: UMNL Hemiplegia or paresis contralateral. If frontal lobes are affected bilateral ---- pts may have paraplegia or paresis b/ Sensory: PCS Deep & Fine. -Parasthesia and tingling sensation, radiating on arms –back – legs – on flexion of ptn neck due to dorsal column Nuclei involvement. BARBER’S CHAIR OR LERMITTS SIGN. Lermitts Sign : Electrical shock Runs down back & radiated to limbs With bending neck forward. D/D 1-Cervical cord compression 2–Syringomylia edema in spinal cord canal compression on PCT. 3-Sub-acute degeneration of spinal cord fibrosis Stretch of PCT. c/Cerebellum: dystaxia and other cerebellar sign. d/Frontal: Euphoria or depression 3/ Spinal Cord: a/ Sub-acute degeneration of spinal cord b/ Urinary Dysfunction: Sphincter disturbance. Common in male Common Presentation of MS: -Optic Neuritis & 6th CN palsy (False Localizing Sign) -Spinal cord lesions. -Brain stem lesions. -R&R Sensory lesions.- By Dr : Abdulraouf Abdullatif Inv: 1/Visual Evoked potential: (delay) used for Subclinical Dx. 2/MRI: 1st and most sensitive (White abnormal patches). 3/Lumbar Puncture: T – Lymphocyte (Pleocytosis) Protein. Oligoclonal band: IgG 80% (Heavy Chain). 4- CT scan Rx: 1/Acute Relapsing: -Steroid ((methyl prednisolone)) 1mg-IV x 3days. 2/Rx Complication. 3/Vit B12. 4/ For prevention and relapsing: 1/interferon beta is the best b/c less s/e. 2/Azathioprine: drugs progression not cure. Prognosis: good 30% = 10yrs. 50% = 15yrs. Poor prognostic factors: 1/Progressive type. 2/Frequent relapse. 3/Male. 4/Age>40 or Upper limb (Distal to proximal). Ptn complain of fatigability difficulty from raising from sitting position or climbing stairs. S&S of LMNL (Loss of Reflexes). By Dr : Abdulraouf Abdullatif 2/Cranial Nerves Involvement: 7th (Bilateral), 3th, 4th, 6th & also bulbar Msc. Complaining of (Diplopia, Drooling saliva, regurgitation& dysphagia). 3/Sensory: Parasthesia & Numbness (Distal to proximal) LLUL. 4/Spinal Cord: -Urinary symptoms (Retention). 5/Dyspnea: -Late in course suggestive of diaphragmatic & intercostal Msc Weakness RFII Death. -may occur within hrs of presentation. Inv: 1/Nerve conduction studies: Abnormal (Confirm Dx). 2/Electromyogram (EMG): Normal. 3/CSF: Albumin-Cytology Dissociation ( Pr & normal cells) 4/Identify the Underlying cause: Stool Analysis & Bronchoalveolar lavage. Rx: 1/High dose IV gamma globulin during acute phase to reduce sy mptoms (eliminate formed AB). 2/Plasma phoresis or exchange (Useful in Rx 1st week). 3/Ventilator support if respiratory Muscle is affected. 4/physiotherapy & occupational. 5/Vit B12. N.B: steroid has no role b/c no further formation of Abs. By Dr : Abdulraouf Abdullatif Myasthenia Graves. Def: Its progressive neuromuscular junction disorder due to ( effect on receptor). Pathophysiology: Action potential stimulate Ca++ gated channels influx of Ca++ which is bind to vesicle Ach vesicle bind to membrane of nerve ending exocytosis of Ach Ach bind to receptor of Msc end plate Msc contraction after contraction Ach esterase destruction of Ach. -in case of MG receptors are affected by Abs leading to: Breakdown of Ach receptors. Accelerate apoptosis of receptors. Blocks of Ach receptors. *Causes of Ab: 1/Autoimmune: IgG Female>Male. (20-40yrs) mainly affect two age group 15-50yrs & >60yrs. +ve F/h. HLAB8 HLADrw3. Ass’ with other autoimmune disease (SLE & RA -Thyroid- DMI- Dermatomyocyte). Circulatory Abs: Anti Ach receptor IgG 70%. 2/Thymic Abnormality: Thymoma- Thy mic hyperplasia. By Dr : Abdulraouf Abdullatif C/P: *Muscles affects: 1/Extralocular ms + Levetor palpebral superior’s ms Diplopia & Ptosis. 2/Bulbar ms Dysphagia. (Aspiration Pneumonia) 3/Shoulder Gridle proximal ms weakness of UL (weakness of combing hair). 4/Pelvic Gridle weakness ms fof LL weakness on climbing stairs & arising from sitting position. 5/Trunk. 6/Respiratory ms RFII. N.B: there is no sensory loss & complaining of Ms pain. *Msc weakness characteristic: at end of day. After repeated ms work exercise R & R Course. Use of some drugs (D-pencillamine , Aminoglycosides, Ciprofloxacin, Propranolol & Quinine). Inv: 1/Edrophonium test: (Tension test) short acting. Anticholinesterase Improve sy mptoms within 30sec (best test). 2/EMG: decremental response. 3/Ab: *Anticholine receptor Ab (80%) Auto immune. *Ant skeletal ms Ab (20%) Thymoma. 4/CT for thy moma. 5/Screening for other autoimmune. **Dx confirmed by: ptn can’t perform continuous voluntary contraction. By Dr : Abdulraouf Abdullatif Rx: 1/Pyridostigmine (Long Acting Anticholinesterase). 2/ CT or CXR +ve Thymoma -ve Ab Autoimmune -Resection. -Steroid. 3/Immunoglobulin. 4/PlasmaPhrases or exchange. *S/E of Pyredostigmine: -Cholinestrase crises salivation – sweating – small pubil – lacrimation – urination – Diarrhea – Gastric Colic. * Myasthenia Crises: life threating due to respiratory failure type II, sudden Rapid progressive weakness especially respiratory ms. Severe dyspnea Treated by Emergency Intubation & Mechanical ventilation + plasma pharesis. Pyridostigmine has no Role b/c its long acting (late onset). ***Eatan Lambert Syndrome : Myasthenia disorder ass’ with malignancy (sq.c.c). -C/P: -Ms weakness trunk & pelvic girdle. -Bulbar involvement rare, auto immune involvement. -Cause: Ab to Ca++ channel. -Inv: EMG. -Rx: 3.4 Diaminopyridine & Iv IMMUNOGLOBULINE. By Dr : Abdulraouf Abdullatif Extra pyramidal System (Basal Ganglia) *General Anatomy: basal ganglia are formed of group of nuclei separated by anatomy. 1/Caudate Nucleus: Cholinergic Nucleus (Ach Rec). Corpus Striatum 2/Lentiform Nucleus: Dopaminergic Nucleus (Dopamine receptor). 3/subthalamus. 4/Substantia Nigra, secrete Ach & Dopamine. Functional related Nuclei. *Function of basal ganglia: 1/Subconscious control of voluntary movement. 2/Control of rapidly of movement. 3/Control of intensity of movement. 4/Control of skilled movement. 5/Control of Muscle tone. **Ach pathway stimulation of Muscle tone ( Function of basal ganglia). **Dopamine pathway inhibition of muscle tone ( function of basal ganglia). Disorder of basal ganglia Dyskinetic Syndrome. Akinetic Rigid Syndrome -Chorea. (Dancing movement). -Parkinsonism. (Caudate controls) -Athetosis. 1) Chorea: Due to lesion in caudate Nucleus, its small amplitude involuntary rapid purposeless (Dancing Movement). *Causes of Chorea: 1/R.F: Sydenham’s chorea. 2/Hereditary. 3/Wilson’s disease. 4/kernicterus. 5/Drugs(Dopamine agonist, L-dopa, Phenothiazine’s & TCA.). 6/Thyrotoxicosis. 7/Hypothyroidism. 8/Hypoglycemia. 9/Huntington’s Chorea. 2) Athetosis: due to lesion in Lentiform Nucleus, its Jerky spasmodic involuntary writing movement affecting distal parts mainly. By Dr : Abdulraouf Abdullatif Parkinsonism Def: Clinical syndrome due to defect in neuro striatal Dopaminergic pathway due to 1- Degeneration of substantia Nigra Depletion of Dopaminergic Neurons 2- decrease receptor sensitivity 1ry Idiopathic (Parkinsonism disease) 2ry Parkinsonism Most common. Toxins (CO, Mg, Poising ,Drugs). Unknown etiology but commonly (Aging). Trauma. >65yrs.. Tumors: 1ry & 2ry. Less commonly in Cigarate smoking. Total viral encephalitis. Female = Male VODKA Vascular –CVA. Orthostatic Hypotension +Atonic bladder. Rare Dementia + Vertical gase. Kaiser Fleisher Ring (Wilson’s Dis). Apraxic Gait (Hydrocephaly). C/P: 1/Flexed Posture: Flexion of back, hip, knee & elbow (rigidity) Flexion of wrist & static tremor Resting (Pill rolling = early unilateral but late may be bilateral ). 2/Dysarthria: Monotonous speech (Voice become soft, Rapid & indistinct) 3/Loss of facial expression: (Mask Face) Hypomania. 4/Loss of blinking of eye but eye movements are normal. 5/Greasy Skin: Due to Sebum Production. 6/Drooling of saliva b/c of mandible tremor. By Dr : Abdulraouf Abdullatif *Other Examination: 1/Glabellar Tap: Tap the forehead just above the bridge of Nose, Repeatedly if normal will stop. if Parkinsonism, blinking will continue (Myerson Sign). 2/Writing: small hand writing (Micrographia). 3/Motor: a) by Inspection Ms wasting, No Fasciculation. b) Tone: -Tone (Hypertonia) Rigidity. -Lead Pipe (Continues). -Cogwheel Intermittent with tremor Wrist. C) power & Reflexes usually remain normal. 4/Gait: Extrapyramidal gait, festinating, shuffling, paarkinsonian gait: a))Slow to start walking. B))Short stride. C))Rapid small steps. d)) tendency to run & fall. E)) loss of swinging. F)) Impaired balance on turning. *Common presentation: Depression + Constipation + Difficulty in movement. *Rare Presentation: Insomnia, Anosmia, Visual Hallucination, Urinary frequency + urgency, dementia. -Difficulty in movement. Dx: -Hypomania. Bradykinesia –Loss f arm swinging. –Flexed posture. Tremor pill or rolling. Rigidity –Hypertonia. *May found pathological changes: 1/Neuronal loss with depigmentation of substantial Nigra. 2/Loewy Bodies: Esinophilc, cytoplasmic inclusion in neurons). By Dr : Abdulraouf Abdullatif Rx: 1/Reassurance & Psychological support. 2/Drugs it’s based on either to give Dopamine or to decrease action of Ach. *Functioning: can do daily activity. -if < 60 yrs Anticholinergic (Benzahexole). s/e (dry mouth, blurred vision, facial flushing, constipation) –if >60yrs dopamine agonist (Amantadine). s/e postural hypotension, so change to Monoaminooxidase inhibitor Type B. *Non functioning: can’t do daily activity. -Levo-dopa + Carpidopa (-decarboxylase). s/e: 1st pass metabolism in liver, on off phenomena & postural hypotension. -Dopamine Receptor agnist (Bromocriptine). 3/ Physiotherapy. 4/Occupational. By Dr : Abdulraouf Abdullatif Lumbar puncture Lumbar puncture is a process by which a spinal needle is used to obtain sample of CSF indications : 1- infections (meningitis or encephalitis), subarachnoid haemorrhage, 2- inflammatory conditions (multiple sclerosis, sarcoidosis & cerebral lupus) 3- neurological malignancies (carcinomatous meningitis, lymphoma and leukaemia); 4- measure CSF pressure (in idiopathic intracranial hypertension). 5- part of the procedure of myelography 6- therapeutic procedures, either to lower CSF pressure or to administer drugs. Procedure: Lumbar puncture involves inserting a needle between lumbar spinous processes (usually between L3-L4 or L4-L5) through the dura and into the CSF under local anaesthetic. Contra indecations: 1- If there is a space-occupying lesion this can result in coning, 2- clinical suggestion of raised intracranial pressure (papilloedema), 3- depressed level of consciousness 4- thrombocytopenia or disseminated intravascular coagulation, 5- warfarin or heparin therapy 6- Hypotension 7- infection near site Side effects: 1- headache (30%), 2- pain over the lumbar region 3- Infections 4- bleeding 5- coda equine syndrome By Dr : Abdulraouf Abdullatif Analysis: 1-Intracranial pressure measurment 2- a naked eye examination of the CSF, 3- centrifugation to determine the colour of the supernatant 4- biochemical analysis (glucose, total protein, and protein electrophoresis to detect oligoclonal bands), 5- microbiological analysis ( PCR for herpes simplex or tuberculosis), 6- immunology (paraneoplastic antibodies) 7- cytology (to detect malignant cells). By Dr : Abdulraouf Abdullatif Meningitis Acute infection of the meninges Causes of meningitis: N.B: Protozoa and parasites: Toxoplasma , Amoeba Fungi: Cryptococcus Candida Infective Bacteria Viruses Non-infective ('sterile') 1- Neisseria meningitidis 1- Enteroviruses 1- Malignant disease: 2- Streptococcus 2- Mumps cancer, Leukaemia pneumonia 3- Influenza Lymphoma 3-Listeria monocytogenes 4- Herpes 2- Inflammatory disease: 4- Mycobacterium 5- Varicella zoster Sarcoidosis SLE tuberculosis 6- Epstein-Bar Behçet's disease 5- Staphylococcus aureus 7- HIV 6- Haemophilus influenzae CP: 1- toxemia: pyrexia, headache, drowsiness, Meningococcal meningitis is associated with a purpuric rash in 70% of cases. Shock, DIC, Renal failure, Peripheral gangrene, Arthritis, Pericarditis 2- Meningism : *stiffness of the neck, often accompanied by other signs of meningeal irritation including: * Kernig's sign (extension at the knee with the hip joint flexed causes spasm in the hamstring muscles) *Brudzinski's sign (passive flexion of the neck causes flexion of the hips and knees). Meningism is not specific can occur in subarachnoid haemorrhage. By Dr : Abdulraouf Abdullatif 3- Signs of increase ICP: Frontal Headache - Impairment of conscious level – Papilloedema - Vomiting, bradycardia, arterial hypertension False localising signs 6th cranial nerve lesion (unilateral or bilateral) Bilateral extensor plantar responses 4- Signs of focal neurological defect : convulsion ( late in adults ) , focal paralysis , coma Dx: 1- CBC , ESR, CRP 2- U&E 3- Blood sugar level 4- CT scan to exclude mass or increase in ICP 5- CSF analysis to confirm Dx & cause Rx: Bed rest specific Antipyretic O2 & fluids Treatment of Bacterial meningitis : 1. Patients with a typical meningococcal rash = Benzylpenicillin 2. Adults aged 18-50 years without a typical meningococcal rash= Cefotaxime or Ceftriaxone 3. Patients in whom penicillin-resistant pneumococcal infection is suspected As for (2) but add: Vancomycin or Rifampicin 4. Adults aged over 50 years As for (2) but add: Ampicillin or Co-trimoxazole 5. Patients with a clear history of anaphylaxis to β-lactams= Chloramphenicol plus Vancomycin Treatment of viral meningitis : no Rx except if herpes give acyclovir Treatment of TB meningitis : anti tuberculosis drugs Prevention : close contacts especially children, should be given 2 days of oral rifampicin In adults, a single dose of 500 mg of ciprofloxacin is an alternative. By Dr : Abdulraouf Abdullatif Headache Headache ICP Tension Headache Migraine Cluster Site: Generalized. Generalized. Half (Unilateral). Half (Unilateral) Severity: Mild to Mild to Severe. Severe. Moderate. Moderate (Dull ache) Onset: Slowly. Slowly. Sudden. Sudden. Character: Non pulsatile. Non pulsatile Pulsatile d/t VD. Pulsatile. Course: Morning >Evening. Even > Morning. Raid progressive Progressive. Radiation: No Occiput forward. No. Per orbital. Reliving -upright position. Avoidance of -Analgesia. -Drugs. -Analgesia. Stress. -pregnancy. -100% O2. Aggravating -Bending forward. -stress. -Stress-hunger- -Smoking. -cough. -anxiety. Chocolate-coffee -Alcohol. -straining. -cheese-noise- light-strong odor -menstruation & OCP. Ass’ Vomiting not No. Vomiting-Aura. -congested eye- Preceded by aura Rhinorrhea- or nausea. Horner. By Dr : Abdulraouf Abdullatif Time Few Hours. Few Hours. 4-72hrs. 45-90min. Rx: -CT & MRI. -Rx stress. -Avoidance RF. -Sumatriptan. -Rx cause. -Avoidance RF. -NSAID. -prophylaxis: -Analgesia. -Analgesia. -Sumatriptan. (Propranolol- -Lactulose. -Ergotamine. verapamil- -Prophylactic: Prednisolone). (Propranolol- Verapamil- Amitryptan). Epilepsy Seizer: abnormal discharge of impulses in the brain due to imbalance between excitatory & inhibitory neurons Epilepsy : Recurrence unpredictable seizers which neurons synchronally active. Trigger factors for seizures causes: 1- Sleep deprivation 2- Alcohol (particularly withdrawal) 3- Recreational drug misuse 4- Physical and mental exhaustion 5- Flickering lights, including TV and computer screens 6- Intercurrent infections and metabolic disturbances 7- Uncommonly: loud noises, music, reading, hot baths Classification: Partial Genaralized By Dr : Abdulraouf Abdullatif Simple Partial Complex Partial Generalized Generalized ( without loss of ( with loss of convulsive non convulsive consciousness ) consciousness ) Motor Grand mal epilepsy Peitimal Sensory Tonic Atonic Visual Clonic Myoclonic Infantile spasm 1- Partial motor seizures Epileptic activity arising in the pre-central gyrus causes partial motor seizures affecting the contralateral face, arm, trunk or leg. Seizures are characterised by rhythmical jerking or sustained spasm of the affected parts. They may remain localised to one part, or may spread to involve the whole side (march Jacksonian seizure). More prolonged episodes may be followed by paresis of the involved limb lasting for several hours after the seizure ceases (Todd's palsy). 2- Partial sensory seizures Seizures arising in the sensory cortex cause unpleasant tingling or 'electric' sensations in the contralateral face or limbs. A spreading pattern similar to a Jacksonian seizure may occur 3- Partial visual seizures Occipital epileptic foci cause simple visual hallucinations such as balls of light or patterns of colour. Formed visual hallucinations of faces or scenes arise more anteriorly in the temporal lobes. 4- Complex partial seizures they arise from the temporal or, less frequently, the frontal lobe Characterized by Aura preceding attack episodes of altered consciousness without the patient collapsing to the ground,. Automatism (stare blankly, often blinking repetitively, making smacking movements of their lips, or displaying, picking at their clothes. After a few minutes, consciousness returns but the patient may be muddled and feel drowsy for a period of up to an hour. By Dr : Abdulraouf Abdullatif 5- Tonic clonic seizures ( GRANDMAL ) commonest type -- Prodormal phase: ( hours or days) = pts feels anxious unease -- The 'aura' phase: (sec. to minutes) = twitching of muscles & abdominal discomfort & -- The tonic phase : ( 10 -30 sec.) = flexion ,adduction of arms , extension of legs , rolling of eyes hallucinations, falling down, respiration is arrested and central cyanosis may occur. –- The clonic phase: ( less than 5 minutes) = alternating contractions & relaxations , tong biting, forty sputum, incontinence -- The post ictal phase: ( hours to days) = patient then gradually regains consciousness, but is in a confused and disorientated & usually feels terrible, may have a headache and will often want to sleep. Dx: Confirm Dx by clinical history from witnessed people & abnormal EEG , EEG may be normal in-between attacks , & 2% of normal people may have abnormal EEG CT & MRI: done if 1- epilepsy after 20 y 2- focal neurological defect 3- faliuer of Rx Detect cause Rx: 1- education of pts about disease & risk factors 2- Anti epileptic drugs -Tapering gradually need so need time & do not stop the drug suddenly. 1st Drug 3mounths By Dr : Abdulraouf Abdullatif Responded Not responded 2yrs – 4yrs without attacks, 2Drugs initially (3mounths) tapering slowly within 6mounths -1yr. if respond, draw one drug then (2- 4yrs) *Simple Partial: If respond gradually draw too. -Tegretol ( carbamazepine.) -Depakaine ( Na+ Valpoate ) *Complex Partial: the same. *Grandmal: DOC (Depakaine + lamotregen). *Unknown Type: Broad spectrum Depakaine. N.B: Private car use Single seizure Cease driving until 1 year has passed without recurrence. Epilepsy (i.e. more than one seizure over age 5 years) Cease driving Licence until 1 year has passed without recurrence Licence will require renewal every 3 years thereafter until patient is seizure-free for 10 years Withdrawal of anticonvulsants Cease driving during withdrawal period and for 6 months after Vocational drivers (public service vehicles) No licence permitted if any seizure has occured after the age of 5 years until patient is off medication and seizure-free for more than 10 years, and has no potentially epileptogenic brain lesion By Dr : Abdulraouf Abdullatif Status Epileptics Def: Repeated contraction within than 30 min or without regain conscious back. Causes: -Space occupying lesion. –Electrolyte Imbalance. Maintain Air way BY Addmit Pts Oropharangeal tube to avoid air way blocked by ABC tongue BP unstable stable IV colloid 1- Give Diazepam or Lorazepam (DOC) +ve by IV, Rectally or interosseous.But inotropic when give IV, should be slowly to avoid Respiratory arrest. New ----->Midazolam (Spray or Patch). 2- Wait ----->15 min If failed 3- Repeat diazepam or lorazepam 4- Wait ----->15 min If failed 5- phenytoin IV mix with Dextrose saline slowly b/c Bradycardia. 6- Wait ----->15 min If failed 7- phenobarbitone 8- Wait ----->30 min If failed 9- Generalized Anesthesia (Na thiopentone