Patient name : Manujanath
Age: 56 years
OP no: 2675558
Manjunath, a 56 year old male patient, presented with
• Severe back pain- gradually progressive, non radiating,
increasing intensity to the point where he was unable to
• Inability to stand up from the sitting or squatting position
• Inability to climb up the stairs
• Generalized weakness, easy fatiguability
• Increased swelling of the hands, limbs and face
• Increased salivation and burning sensation of the mouth
All these symptoms began 20-25 days back and has
increased in intensity since then.
• Decreased appetite and weight loss of >10 kg over 6
No c/o fever/ cough/chest pain/ SOB/ bleeding
manifestations/ vomiting/ loose motion /dysuria.
No c/o tingling numbness/ slipping of sandals from the feet/
inability to comb hair/ to eat food with his hands/ altered
sensorium/ drooping of eyelids in the evening.
Known case of DM since 17 years (on Tab. Glimepiride-
Metformin) and chronic Pancreatitis with pancreatic
pseudocyst s/p sphincterotomy and stenting. No h/o thyroid
problems or steroid intake.
Chronic smoker and alcoholic who had his last drink 20-25
Other medications (prescribed when he visited OPD on
Cap. Panlipase, T. lasix 20mg OD, Cap. Zevit
Poorly built, poorly nourished
Pallor+++, Icterus+, Anasarca, Glossitis- bald beefy tongue
B/L entropion and watering of both eyes
Pulse: 99/min BP: 120/70 mmHg
Saturation : 95% on RA RR:18/min
PA: soft, non tender BS+
HMF: Conscious oriented, speech was fluent
Cranial nerves: no deficits
Power: Able to move his limbs, Pt unable to sit up and get out of
bed without support, Pt able to walk without support.
5/5 in upper limbs
Hip and knee - flexion and extension: 3/5 on left, 4/5 on right
Ankle dorsiflexion and plantar flexion: 5/5
Sensory system intact
DTR +, both plantars flexor
• True weakness is the inability to perform a desired
movement with normal force because of a reduction in
• It has to be distinguished from malaise due to medical
conditions – perceived
FAMILIAL PERIODIC PARALYSIS
glycogen storage / lipid storage
DRUG-INDUCED – glucocorticoids, colchicine, penicillamine, etc
CUSHING’S SYNDROME – protein degradation, mitochondrial alterations,
decreased sarcolemmal excitability
POLYMYOSITIS- proximal weakness with chronic inflammation of muscles,
esophageal dysmotility, foot drop (u/l or b/l), +/- ILD, mainly females
DERMATOMYOSITIS- polymyositis with gottron’s lesions, calcinosis of skin, joints
and vasculitis, mainly females
INCLUSION BODY MYOSITIS- polymyositis with distal muscle involvement
MYOSITIS OSSIFICANS- heterotropic calcification at sites of blunt trauma, within
muscles mainly quadriceps, glutei, pectoralis, intercostal spaces
RHABDOMYOLYSIS sec to infection, crush injuries, medications, toxins, etc.
HYPOTHYRODISM (abnormal glycogen accumulation, type 1 fibre atrophy)
HYPERTHYROIDISM (AchE degradn and MEP structural changes- increased firing-
• Alcoholic myopathy, in acute or chronic forms, are rare.
• Only 8 patients out of 510 patients studied showed some
form of alcoholic myopathy, mainly due to an excessive
accumulation of triglycerides in the muscles.
• Seen more prominently in patients who drink over 100
gms of alcohol for a period of more than 3 years is at
• The relation between alcohol and muscles-
• Acute rhabdomyolytic process
• Swollen tender muscles accompanied by severe proximal
• May cause acute renal failure – dialysis.
• Spontaneous recovery is the rule rather than the exception i.e if
patient withdraws from alcohol successfully.
• Pathophysiological basis unknown.
British Medical Journal, Volume 288, Page 5 84, 25 Feb1984.
• Decrease in type 2 (fast twitch,
anaerobic, glycolytic) muscle fibers
• Acetaldehyde adducts – contractile
defects and muscle weakness
• Loss of dystrophin
• Reduced rates of muscle synthesis
• Increased production of cholestrol
• Generation of free radicals + Low
serum levels of selenium and
60% of 150 subjects studied had some form of
skeletal muscle damage on biopsy- more
common in western hemisphere.
TYPES ONSET GENDE
Duchenne Most common,
Males Dystrophin glycoprotein complex defect – disruption of outer muscle
memb- weakness and wasting, early demise
Becker’s Less severe
Males Partially functional dystrophin, survival into old age
Congenital Gen weakness + joint deformities, slow progression, early demise
Emery Dreiffus Childhood Gen weakness, wasting leading to teenage contractures, distal to
proximal progress, sudden death due to arrhytmias, strokes
Limb girdle Recessiv
Both Affects proximal muscles, normal life with
death due to cardio-pulmonary
Myotonic Dominant Delayed relaxation, wasting, weakness
Oculopharyngeal Affects face, eyes and pharynx f/b proximal muscle
weakness, 40-70 yrs
• GRBS: 121 mg/dl
• ECG: Sinus tachycardia
• MRI spine after Neurology reference
• Planned for admission.
pH pCO2 Hb Na K Cl Lac Creat Hco3 Hct
7.446 37.6 6.0 127 3.3 97 5.1 0.95 25.5 19.0
• CLD with dilated portal veins
• Chronic calcific pancreatitis
• Moderate ascites
MRI spine: C4-C7 and L2-S1 disc bulges causing thecal
compression and neural compromise.
OGD: Esophageal ulcer (awaiting biopsy report) with
ENMG: severe motor and sensory neuropathy