You are again asked to see a patient with GBS. A young man in his 30's, does not seem perturbed by his acute onset of weakness of lower limbs. He says he has been through it on many occasions before. This particular bout was triggered after a hearty meal at a wedding. Thoughts?
An important differential to GBS are the Channelopathies. This gentleman had low levels of Potassium, and correction of the same completely reversed his symptoms! On evaluation, he was diagnosed with a Channelopathy
Simplified Approach

#Neurology
Hypokalaemia is notorious to cause neurological weakness often mimicking GBS. However clinical pointers for it are
- Recurrent Attacks
- Triggered by Alcohol/Carbs
- No Bulbar/ Facial Involvement
-Preserved reflexes (Can have areflexia!)
-Rapid (to come and go)
-Normal CSF
Hypokalaemia may be due to a primary Channelopathy, which are rare diseases, for more commonly secondary to an underlying cause of hypokalaemia. So in a patient with HypoK paralysis:-
Step 1: Is there any Acid Base Abnormality?
If NO -> think of the primary channelopathies

If YES
Step 2:
Metabolic Acidosis:
Distal RTA (eg Sjogren's: have seen a number of such patients!)
Diarrhea

Metabolic Alkalosis:
Hyperaldosteronism
Bartter/Gitelman
Thiazide Use
Secondary causes are most common, hence ask for
Dry Eyes/Mouth, arthralgia (Sjogren)
GI disturbances
Hypertension in Young
Detailed Drug history
Coming to the Channelopathies
Theseinclude :
1. Hypokalemic Periodic Paralysis (Calcium Channel)
2. Hyperkalemic Periodic Paralysis (Sodium Channel)
3. Anderson Tawil Syndrome (Potassium Channel)
4. Thyrotoxic Periodic Paralysis (Potassium Channel) (most common in India)
Hypokalemic Periodic Paralysis
- Recurrent episodes
- triggered by high carb diet/alcohol
- can eventually progress to a fixed weakness
Rx: Acetazolamide, Spironolactone Potassium Supplement Avoid High Carb/alcohol
Hyperkalemic Periodic Paralysis

More frequent and shorter attacks
MYOTONIA is present
Triggered by fasting (Contrast with hypo)
Cardiac involvement (high K)

Rx: Glucose / Calcium

Caveat: Potassium Levels can be normal when tested, so normal K does not rule out the diagnosis
Andersen Tawil Syndrome

1. Episodic Weakness
2. Ventricular Arrythmias
3. Dysmorphic Facies
Thyrotoxic Periodic Paralysis

Basically via Hypokalemia, so similar features
May have evidence of Thyrotoxicosis
Drug of Choice: Beta Blocker/Propranolol
Coming to our patient
No cranial nerve inv.
Recurrent symptoms, triggered by heavy meal, low potassium level prompted suspicion of Hypokalaemia.
No Acid Base Abn]
Sketchy family history of similar complaints
No evidence of myotonia, sicca, GI abnormalities, HTN
Thyroid:Normal
Potassium corrected and he is discharged on Acetazolamide, and counselled about diet/alcohol
So far no recurrences !
Here is yet another mimic of GBS! Every patient with GBS should be evaluated for this. It is a lot more common than we realise, and easy amenable to treatment, indeed, so one may be more cautious for a deadly arrhythmia

#MedTwitter #MedEd #NeuroTwitter
Src: hkpp.org
From UpToDate

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Mar 9
Young boy w/ acute onset quadriparesis with areflexia, admitted to ICU with "GBS". You happen to glance at Urine Bag. something is off! The old urine is darker!? The patient is squealing with abdominal pain. Relatives tell you- seizures in the past
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#cinema #neurotwitter #MedTwitter
Simplifying , for carrying out bimanual planned movements, we need a Supplementary Motor Cortex (SMA) (left frontal lobe). This communicates to the opposite side via the corpus callosum. Lesions in any will impair proper bimanual function and cause an “alien limb”#neuroanatomy
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Affects the dominant hand
Can be due to a #stroke, #degeneration

My patient impulsively grabs my hand (with his right hand) despite me telling him not to!
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