by ANU.S MBBS 2006 Kannur Medical College

A male patient, Mr. Arun 40 yr old business man hailing from a middle socioeconomic status came with the following chief complaints ◦ Weakness of right Lower Limb for 1 week ◦ Numbness of rt foot for 1 wk ◦ Defective vision for 1 week

 The patient was admitted with history of weakness of right LL of 1 week duration ; gradual in onset and progressive in nature  There is associated numbness of right foot & dragging of rt foot while walking for 1 wk  H/o defective vision for 1 week  No h/o deviation of angle of mouth,headache, memory loss, disorientation

PAST H/O ◦ h/o similar complaints on the opposite side (l t side) and h/o medication from Manipal ◦ No h/o DM, HT, EPILEPSY and TB PERSONAL ◦ Was a smoker for 15 yrs ◦ Was an alcoholic for 15 yrs ◦ Takes Mixed Diet ◦ Appetite decreased ◦ Bowel and bladder normal ◦ Sleep normal FAMILY H/O ◦ No h/o similar complaints in family ◦ No h/o DM, HT,neuropathy,ataxia, epilepsy

GENERAL EXAMINATION  Patient is conscious,co-operative, well oriented, moderately built and poorly nourished VITAL SIGNS  Pulse rate-74 beats/min  BP-130/80 mmHg ;rt arm; supine position  RR-18 cycles/min  Temp-afebrile

CNS EXAMINATION  Patient is alert with normal speech RELEASED REFLEXES -absent EXAMINATION OF CRANIAL NERVES  Visual Acuity –B/l Reduced  Hearing - Normal Examination of motor system  Strength of muscle LtRt UPPER LIMB4+ LOWER LIMB4+3+

 Plantar -extensor on right  Other superficial reflexes normaI  Deep reflexes-normal  Ankle reflex-normal  Gait –dragging of rt foot Test for coordination and movements  Finger nose test-positive  Heel to knee test-negative  No involuntary movements

 Visual acuity –Reduced B/l Optic atrophy present  Hearing –Normal Examination of sensory system  Decreased touch & pain over rt LL  Position sense-normal  Romberg’s sign-negative  Dragging of rt foot CVS, RS - WNL

 VISUAL EVOKED POTENTIAL (VEP) STUDY Prolonged P100 latency of evoked response on both eyes (rt > lt) ; B/L delay in conduction  RBS -108 mg/dl  MRI SCAN SHOWS – MULTIPLE PERIVENTRICULAR HYPERINTENSITY IN T2 & FLAIR IMAGES

3 out of 4 of the following  1 gadolinium- enhancing brain or cord lesion or 9T2 hyperintense brain and /or cord lesion if there is no gadolinium- enhancing lesion  One or more infratentorial or cord lesion  One or more juxtacortical lesion  Three or more periventricular lesion

 Pt. had neurological deficit disseminated in time  He has optic nerve involvement & multiple periventricular hyper intensities in MRI ALL THESE FEATURES ARE SUGGESTIVE OF MULTIPLE SCLEROSIS

 INJECTED WITH 1g METHYL PREDNISOLONE FOR 5 DAYS  FOLLOWED BY STEROID - 2 WKS  INJ; REBIF (INTERFERON BETA 1A) SUBCUTANEOUSLY THRICE A WEEK CONDITION AT DISCHARGE; IMPROVED

 Demyelinating disease  Characterised by neurological deficits due to involvement of optic nerves, cerebrum, cerebellum, brain stem & spinal cord  Usually affects women (20-35 yrs) & men ( yrs)  Sometimes – familial IMMUNOPATHOGENESIS In MS it is evidenced by ; 1. Presence of immune reacting cells 2. Inflammatory cytokines in serum, CSF & Brain 3. Immunomodulators are effective therapeutically 4. MS is intiated by immune cells in animal models

CLINICAL PRESENTATIONS Based on its clinical course, classified into; 1. Relapsing; remmiting type (R-R type) most common (85%) 2. Progressive type ; deterioration continues for atleast 1yr most drammatic symptom ; visual loss  Weakness or numbness in one or more limbs  Other presntns ; unsteadiness of gait, brain stem symptoms – diplopia, vertigo, vomiting, bladder disturbance  Dementia,aphasia, seizures, & extrapyramidal symptoms are rare

 Once established, the disease is characterized by remissions & relapses at multiple sites at variying intervals  Post column deficits & pyramidal involvement are common  Polysynaptic reflexes such as superficial reflexes may be affected early  Optic atrophy,spastic paraparesis, cerebellar signs like intention tremor or ataxia & internuclear ophthalmoplegia – distinctive findngs  B /L trigeminal neuralgia is characteristic of MS

 Rarely combination of cerebral,brainstem & spinal manifestaton- rendering the pt. stuporous or comatose. Such cases death may occur DIAGNOSIS  Cinically 2 attacks separated in time by atleast 1 month with cinically evidence of atleast 2 separate lesions in the CNS or 2 attacks with cinically evidence of 1 & investigational evidence of another separate lesion.  CSF show lymphocyte pleocytosis upto 20 cells /cmm- slight rise in total protein - increased IgG component - electrophoresis – oligoclonal bands  Early stage- diagnosis is done by recording the evoked potentials by visual, auditory & somatosensory stimuli  MRI- plaques of demyelination

3 categories  Treatment of exacerbations  Disease modifying therapy  Symptomatic treatment

TREATMENT OF EXACERBATIONS IV Methyl prednisolone 1gm/day for a 3or 5 day course followed by a rapid tapering course of oral steroids  Plasmapheresis – fail to respond to corticosteroids DISEASE MODIFYING THERAPIES  Interferonβ 1b  Inf β1a  Glatiramer acetate  Mitoxantrone  Repetitive course of steroids  Selective therapy – natalizumab 300 mg i.v once in 4 wks  Fingolimod  Bonemarrow or stem cell transplantation

SYMPTOMATIC TREATMENT  Amantadine - fatigue  Baclofen, dantroline, diazepam- to allay spasticity  Clonazepam & high dose INH- to allay intention tremor  Oxybutinin and propantheline – to reduce urinary frequency and urgency.