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NEUROLOGICAL PRESENTATION:
METABOLIC ORIGIN
DR SUDHIR KUMAR
MD (Med) DM (Neuro)
Consultant Neurologist
Apollo Hospitals, Hyderabad
NEUROLOGY SPECIALITY
Opinion poll:
1. Neurology is:
a) Very difficult, b) Easy
2. Neurological disorders are mostly:
a) not treatable, b) treatable
3. Neurological problems can be handled by gen
physician:
a) No, b) Yes
RAPIDLY PROGRESSIVE
QUADRIPARESIS
• 45-year old man presented with acute onset,
rapidly progressive quadriparesis: 1 day
duration,
• No sensory or bladder symptoms
• All DTRs absent
• Cranial nerves- normal
POSSIBILITIES
• GUILLAIN BARRE SYNDROME
• HYPOKALEMIC PERIODIC PARALYSIS
NCV may be abnormal in hypokalemia!
INTRODUCTION
Electrophysiological abnormalities reported in
hypokalemic periodic paralysis (HPP) include
reduced compound muscle action potential (CMAP)
amplitude during a paralytic attack, increased
CMAP amplitude 5 minutes after maximal muscle
contraction, progressive reduction in amplitude 20-
40 minutes after rest(1) and rarely redu
nerve action potential (SNAP) am
Sensory nerve conduction abnorm
reversed with hypokalemia correction a
ment in muscle weakness have been
however, similar findings in motor nerve
studies have been uncommonly re
present a patient with reversible motor
abnormalities.
CASE REPORT
A nine-year old girl with distal renal tub
due to nephrocalcinosis presented w
areflexic quadriparesis of four hours dur
was no sensory loss, cranial nerve in
bladder disturbance or higher function
She was evaluated for electrolyte ab
(suspecting a possible diagnosis of HPP
the reports were still pending, she unde
conduction (NC) study. The NC stu
significant reduction in CMAP ampli
motor nerves. However, the dista
conduction velocities and F-wave lat
within normal limits. Sensory nerve act
(SNAP) amplitudes were also normal. B
electrophysiological findings, an alterna
of acute motor axonal neuropathy (A
of Guillain-Barre syndrome (GBS)
considered. With administration of the
of potassium, the patient showed dram
improvement. The serum potassium rep
available and was 2 mmol/L. Based
original diagnosis of HPP with quadr
confirmed. Nerve conduction (NC) s
repeated 2 hours after the initial study a
hours later, by which time the patient’s m
was back to normal. Repeat NC studies
to be normal.
DISCUSSION
Reversible electrophysiological abno
sensory nerve function have bee
earlier(2). A prospective study in ten p
INDIAN PEDIATRICS 54 VOLUME 45__
JANU
Reversible Electrophysiological
Abnormalities in Hypokalemic
Periodic Paralysis
GARIKAPATI RAJSHEKHER
SUDHIR KUMAR
SUBHASHINI PRABHAKAR
From the Department of Neurological Sciences, Apollo
Hospitals, Hyderabad, India.
Correspondence to: Dr Sudhir Kumar, Consultant
Neurologist, Apollo Hospitals, Jubilee Hills,
Hyderabad 500 033, Andhra Pradesh, India.
E-mail: drsudhirkumar@yahoo.com.
Manuscript received: May 24, 2007;
Initial review completed: July 31, 2007;
Revision accepted: August 24, 2007.
ABSTRACT
Compound muscle action potential (CMAP) amplitude
declines during a paralytic attack in patients with
hypokalemic periodic paralysis (HPP). However, serial
motor nerve conduction studies in HPP have not been
commonly reported. We report a 9-year-old girl with
HPP, who had severely reduced CMAPs in all motor
nerves at presentation during the episode of
quadriparesis. However, the amplitude of CMAPs
increased and reached normal levels as the serum
potassium concentration and motor power returned to
normal state.
Key words: Electrophysiology, Hypokalemic
periodic paralysis, Motor conduction
abnormalities.
C A S E R E P O R T S
MANAGEMENT
• Serum potassium: 2 mEq/L
• IV potassium chloride given
• Patient rapidly improved over the next 24
hours and was able to walk,
• Work up for causes of hypokalemia were
negative.
• Discharged in 3 days with normal neurological
status!
NEUROLOGICAL DETERIORATION
AFTER RECOVERY IN ICU
• 65-year old presented with 2-day history of
delirium,
• Serum sodium 111 mEq/L
• Hyponatremia correction started,
• Patient became alert the next day, with
sodium level 129 mEq/L
• 48 hours later---deteriorated, with confusion,
gaze paresis and spastic quadriplegia.
MRI BRAIN
CENTRAL PONTINE MYELINOLYSIS
• Caused by rapid correction of hyponatremia,
• Maximum permitted correction is 10-12
mmol/L in 24 hour period, 18 mmol/L in 48-
hour period,
• No specific treatment
• Death and permanent neurologic disability are
common.
Teenager with seizures and short
stature
• 18-year old brought with history of epilepsy
since age 3,
• Developmental delay,
• Birth and antenatal history normal.
• Also complained of paresthesias and cramps,
• Examination revealed short stature and short
4th metacarpals and metatarsals
GENERAL EXAMINATION
CT BRAIN
PSEUDOHYPOPARATHYROIDISM
Laboratory investigations
• Low calcium,
• High phosphorus,
• Elevated PTH,
• Normal renal functions.
Management
Calcium, calcitriol supplements
Long-term antiepileptic drugs not necessary.
RECURRENT FOCAL SEIZURES IN ICU
• 75 year old diabetic admitted in ICU with 20-30
episodes of right focal motor seizures per day,
• Mild right hemiparesis (motor power: 3/5),
• Conscious and alert in between seizure episodes,
• CT, MRI brain and CSF analysis normal,
• Seizures persisted despite phenytoin and
midazolam infusion,
• Neurology team consulted.
EPILEPSIA PARTIALIS CONTINUA
STOPPED BY INSULIN
NONKETOTIC HYPERGLYCEMIA
Labs
• High plasma glucose,
• High plasma osmolality,
• Dehydration,
• Absence of ketoacidosis
Management
• Correction of hyperglycemia by IV insulin,
• Rehydration
Proximal myopathy in a young woman
• 25-year old lady with progressive weakness of
all 4 limbs of one year duration,
• LL>UL; Proximal>distal; normal sensory
• Delayed DTRs,
• Muscle cramps+
• Recent weight gain, constipation
• Serum CPK: elevated (>3500)
HYPOTHYROID MYOPATHY
• TSH: 80, low T3 and T4
• Myopathy can be “sole” manifestation of
hypothyroidism,
• Started on levothyroxine supplements,
• Muscle power started improving within 2
weeks
• Patient became completely normal within six
months.
Neurological manifestations of
Hypothyroidism
• Dementia
• Peripheral neuropathy,
• Carpal tunnel syndrome,
• Myopathy,
• Coma (myxedema coma),
• Ophthalmopathy
Progressive Dementia in a Young
Woman
• 23-year old air hostess brought with
progressive memory loss of six months
duration,
• Language and visuospatial dysfunction+
• Poor self care,
• Paresthesias of both feet+
EXAMINATION
• Hyperpigmentation noted over knuckles and
tongue,
• Absent Ankle jerks, reduced sensations in
distal legs/feet, extensor plantar responses.
Hyperpigmentation in B12 deficiency
VITAMIN B12 DEFICIENCY
• Serum vitamin B12 <60 pg/ml
• Elevated homocysteine,
• Positive anti-parietal cell antibodies
• MRI brain- normal; NCV: Sensory neuropathy
• Started on B12 injections
• Reviewed after 3 months- normal cognition.
Decline in Scholastic Performance in a
Child
• 13-year old boy, apparently well until 1 year
ago
• Noted to have decline in scholastic
performance,
• Mild tremors of hands,
• Slurred speech and increased salivation,
• Personality changes
Kayser Fleischer Ring
Investigations
• Low serum ceruloplasmin (<20)
• Increased urinary copper excretion,
• Increased hepatic copper concentration (on
liver biopsy)
• MRI brain- symmetrical hyperintense lesions
in caudate nucleus, putamen and globus
pallidus
MRI BRAIN
WILSON’S DISEASE-Treatment
• Started on chelation therapy with d-
penicillamine,
• Along with zinc sulphate,
• Trihexiphenidyl was given for extrapyramidal
features,
• Child significantly improved during follow up.
Altered Sensorium in a Pregnant
Woman
• 25-year old primigravida at 10 weeks
gestation,
• Brought to the ER with altered sensorium and
confusion of one day duration,
• She has had recurrent/repeated vomiting for
the past one week, with poor food intake,
• No history of fever, seizures or headache.
INITIAL WORK UP
• Seen by gynecologist- diagnosed hyperemesis
gravidarum,
• Serum electrolytes and glucose levels were
normal,
• CT Brain was also normal.
MRI BRAIN
WERNICKE’S ENCEPHALOPATHY
• Caused due to thiamine deficiency,
• Usual settings are chronic alcohol abuse,
malnutrition, hyperemesis gravidarum,
prolonged TPN, post-bariatric surgery,
iatrogenic glucose infusion in a patient with
thiamine deficiency.
• Patient responded to thiamine treatment.
POST POLL
1. Neurology is:
Easy
2. Neurological disorders are mostly:
Treatable
3. Neurological problems can be handled by gen
physician:
Yes
Queries/Comments?
Whatsapp: 9866193953
Email: drsudhirkumar@yahoo.com
Facebook:
https://www.facebook.com/bestneurologist

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NEUROLOGICAL DISORDERS DUE TO METABOLIC DERANGEMENTS

  • 1. NEUROLOGICAL PRESENTATION: METABOLIC ORIGIN DR SUDHIR KUMAR MD (Med) DM (Neuro) Consultant Neurologist Apollo Hospitals, Hyderabad
  • 2. NEUROLOGY SPECIALITY Opinion poll: 1. Neurology is: a) Very difficult, b) Easy 2. Neurological disorders are mostly: a) not treatable, b) treatable 3. Neurological problems can be handled by gen physician: a) No, b) Yes
  • 3. RAPIDLY PROGRESSIVE QUADRIPARESIS • 45-year old man presented with acute onset, rapidly progressive quadriparesis: 1 day duration, • No sensory or bladder symptoms • All DTRs absent • Cranial nerves- normal
  • 4. POSSIBILITIES • GUILLAIN BARRE SYNDROME • HYPOKALEMIC PERIODIC PARALYSIS
  • 5. NCV may be abnormal in hypokalemia! INTRODUCTION Electrophysiological abnormalities reported in hypokalemic periodic paralysis (HPP) include reduced compound muscle action potential (CMAP) amplitude during a paralytic attack, increased CMAP amplitude 5 minutes after maximal muscle contraction, progressive reduction in amplitude 20- 40 minutes after rest(1) and rarely redu nerve action potential (SNAP) am Sensory nerve conduction abnorm reversed with hypokalemia correction a ment in muscle weakness have been however, similar findings in motor nerve studies have been uncommonly re present a patient with reversible motor abnormalities. CASE REPORT A nine-year old girl with distal renal tub due to nephrocalcinosis presented w areflexic quadriparesis of four hours dur was no sensory loss, cranial nerve in bladder disturbance or higher function She was evaluated for electrolyte ab (suspecting a possible diagnosis of HPP the reports were still pending, she unde conduction (NC) study. The NC stu significant reduction in CMAP ampli motor nerves. However, the dista conduction velocities and F-wave lat within normal limits. Sensory nerve act (SNAP) amplitudes were also normal. B electrophysiological findings, an alterna of acute motor axonal neuropathy (A of Guillain-Barre syndrome (GBS) considered. With administration of the of potassium, the patient showed dram improvement. The serum potassium rep available and was 2 mmol/L. Based original diagnosis of HPP with quadr confirmed. Nerve conduction (NC) s repeated 2 hours after the initial study a hours later, by which time the patient’s m was back to normal. Repeat NC studies to be normal. DISCUSSION Reversible electrophysiological abno sensory nerve function have bee earlier(2). A prospective study in ten p INDIAN PEDIATRICS 54 VOLUME 45__ JANU Reversible Electrophysiological Abnormalities in Hypokalemic Periodic Paralysis GARIKAPATI RAJSHEKHER SUDHIR KUMAR SUBHASHINI PRABHAKAR From the Department of Neurological Sciences, Apollo Hospitals, Hyderabad, India. Correspondence to: Dr Sudhir Kumar, Consultant Neurologist, Apollo Hospitals, Jubilee Hills, Hyderabad 500 033, Andhra Pradesh, India. E-mail: drsudhirkumar@yahoo.com. Manuscript received: May 24, 2007; Initial review completed: July 31, 2007; Revision accepted: August 24, 2007. ABSTRACT Compound muscle action potential (CMAP) amplitude declines during a paralytic attack in patients with hypokalemic periodic paralysis (HPP). However, serial motor nerve conduction studies in HPP have not been commonly reported. We report a 9-year-old girl with HPP, who had severely reduced CMAPs in all motor nerves at presentation during the episode of quadriparesis. However, the amplitude of CMAPs increased and reached normal levels as the serum potassium concentration and motor power returned to normal state. Key words: Electrophysiology, Hypokalemic periodic paralysis, Motor conduction abnormalities. C A S E R E P O R T S
  • 6. MANAGEMENT • Serum potassium: 2 mEq/L • IV potassium chloride given • Patient rapidly improved over the next 24 hours and was able to walk, • Work up for causes of hypokalemia were negative. • Discharged in 3 days with normal neurological status!
  • 7. NEUROLOGICAL DETERIORATION AFTER RECOVERY IN ICU • 65-year old presented with 2-day history of delirium, • Serum sodium 111 mEq/L • Hyponatremia correction started, • Patient became alert the next day, with sodium level 129 mEq/L • 48 hours later---deteriorated, with confusion, gaze paresis and spastic quadriplegia.
  • 9. CENTRAL PONTINE MYELINOLYSIS • Caused by rapid correction of hyponatremia, • Maximum permitted correction is 10-12 mmol/L in 24 hour period, 18 mmol/L in 48- hour period, • No specific treatment • Death and permanent neurologic disability are common.
  • 10. Teenager with seizures and short stature • 18-year old brought with history of epilepsy since age 3, • Developmental delay, • Birth and antenatal history normal. • Also complained of paresthesias and cramps, • Examination revealed short stature and short 4th metacarpals and metatarsals
  • 13. PSEUDOHYPOPARATHYROIDISM Laboratory investigations • Low calcium, • High phosphorus, • Elevated PTH, • Normal renal functions. Management Calcium, calcitriol supplements Long-term antiepileptic drugs not necessary.
  • 14. RECURRENT FOCAL SEIZURES IN ICU • 75 year old diabetic admitted in ICU with 20-30 episodes of right focal motor seizures per day, • Mild right hemiparesis (motor power: 3/5), • Conscious and alert in between seizure episodes, • CT, MRI brain and CSF analysis normal, • Seizures persisted despite phenytoin and midazolam infusion, • Neurology team consulted.
  • 16. NONKETOTIC HYPERGLYCEMIA Labs • High plasma glucose, • High plasma osmolality, • Dehydration, • Absence of ketoacidosis Management • Correction of hyperglycemia by IV insulin, • Rehydration
  • 17. Proximal myopathy in a young woman • 25-year old lady with progressive weakness of all 4 limbs of one year duration, • LL>UL; Proximal>distal; normal sensory • Delayed DTRs, • Muscle cramps+ • Recent weight gain, constipation • Serum CPK: elevated (>3500)
  • 18. HYPOTHYROID MYOPATHY • TSH: 80, low T3 and T4 • Myopathy can be “sole” manifestation of hypothyroidism, • Started on levothyroxine supplements, • Muscle power started improving within 2 weeks • Patient became completely normal within six months.
  • 19. Neurological manifestations of Hypothyroidism • Dementia • Peripheral neuropathy, • Carpal tunnel syndrome, • Myopathy, • Coma (myxedema coma), • Ophthalmopathy
  • 20. Progressive Dementia in a Young Woman • 23-year old air hostess brought with progressive memory loss of six months duration, • Language and visuospatial dysfunction+ • Poor self care, • Paresthesias of both feet+
  • 21. EXAMINATION • Hyperpigmentation noted over knuckles and tongue, • Absent Ankle jerks, reduced sensations in distal legs/feet, extensor plantar responses.
  • 23. VITAMIN B12 DEFICIENCY • Serum vitamin B12 <60 pg/ml • Elevated homocysteine, • Positive anti-parietal cell antibodies • MRI brain- normal; NCV: Sensory neuropathy • Started on B12 injections • Reviewed after 3 months- normal cognition.
  • 24. Decline in Scholastic Performance in a Child • 13-year old boy, apparently well until 1 year ago • Noted to have decline in scholastic performance, • Mild tremors of hands, • Slurred speech and increased salivation, • Personality changes
  • 26. Investigations • Low serum ceruloplasmin (<20) • Increased urinary copper excretion, • Increased hepatic copper concentration (on liver biopsy) • MRI brain- symmetrical hyperintense lesions in caudate nucleus, putamen and globus pallidus
  • 28. WILSON’S DISEASE-Treatment • Started on chelation therapy with d- penicillamine, • Along with zinc sulphate, • Trihexiphenidyl was given for extrapyramidal features, • Child significantly improved during follow up.
  • 29. Altered Sensorium in a Pregnant Woman • 25-year old primigravida at 10 weeks gestation, • Brought to the ER with altered sensorium and confusion of one day duration, • She has had recurrent/repeated vomiting for the past one week, with poor food intake, • No history of fever, seizures or headache.
  • 30. INITIAL WORK UP • Seen by gynecologist- diagnosed hyperemesis gravidarum, • Serum electrolytes and glucose levels were normal, • CT Brain was also normal.
  • 32. WERNICKE’S ENCEPHALOPATHY • Caused due to thiamine deficiency, • Usual settings are chronic alcohol abuse, malnutrition, hyperemesis gravidarum, prolonged TPN, post-bariatric surgery, iatrogenic glucose infusion in a patient with thiamine deficiency. • Patient responded to thiamine treatment.
  • 33. POST POLL 1. Neurology is: Easy 2. Neurological disorders are mostly: Treatable 3. Neurological problems can be handled by gen physician: Yes