Metabolic and Immunological Disorders: Metabolic Encephalitis, Subacute Degeneration of Spinal Cord, Alcoholic Neuropathy, Limbic Encephalitis, Too much ACh, Not enough ACh Stimulation

Question 1

Use of the FBC

• why is it used
• what is it diagnostic for?
• how does this condition present?

Answer 1

MOST COMMON INVESTIGATION - cheap, easily available and returns in an hour

• High MCV - alcohol? B12, folate? thyroid?
• High Hb, platelets - TIA, stroke?

diagnostic for SCDC - megaloblastic macrocytic anemia (B12, folate deficient)
-low Hb, high MCV

Causes of SCDC

• alcohol overuse
• nitrous oxide abuse

Pathophysiology and presentation of SCDC
Slowly progressive degeneration of lateral, dorsal column
-weakness, sensory ataxia, tingling, bilateral spasticity, incontinence

Question 2

Metabolic encephalopathy

• presentation and risk factors
• investigations for possible causes

Answer 2

Metabolic
Symptom duration - days
Asterixis, confusion, reduced GCS
No focal neuro deficit, symmetrical exam findings - more likely to be a diffuse issue

CKD, polypharmacy

Bedside 
-BG - hypoglycemia
-urinedip and toxicology - UTI
Bloods
-FBC - anemia, alcohol, thyroid, chronic disease
-LFT, RFT, TFT
-U&E - CKD
-Ca

Question 3

Neuromuscular junction issues
Too much ACh
-presentations and possible cause
Too little ACh stimulation
-presentations, investigations, management

Answer 3

Inhibition of AChE => build up of ACh
Organophosphate poisoning - insecticides => onset within hours
Increased PNS, somatic muscle stimulation
-increased salivation, diarrhea, small pupils, LMN signs, confusion
Managed with atropine and supportive care

AI destruction of AChR => decreased stimulation of somatic muscle
Proximal muscle weakness, diplopia, ptosis, fatigue, difficulties with speech and swallow

Easiest test - icepack
Difficult to access/results take a long time
Bloods - Anti AChR AB
Single fibre EMG - reduced AP amplitude on repeated stimulation

Management - pyridostigmine + IS
-IVIG, resp support if severe

Question 4

Alcohol related neuropathy

-possible issues and how you’d manage them

Answer 4

FBC - megaloblastocytosis
LFT - high GGT, deranged liver enzymes
BAL - high

B12 deficiency => peripheral polyneuropathy (glove and stocking)
B1 deficiency => WE => KS
WE - confabulation, ataxia, eye instability
KS - anterograde, retrograde amnesia

PABRINEX GIVEN BEFORE GLUCOSE

• B1 needed in glucose metabolism
• otherwise, you increase anerobic respiration and cell damage

Question 5

Limbic encephalitis

• presentation, pathophysiology
• key differentials to manage
• key investigations
• definitive management

Answer 5

Paraneoplastic AI condition => attacking NMDA receptors in limbic system
Subacute presentation
-headache
-seizures
-irritability, agitation
-hallucinations, delusions, psychosis
-memory problems

Start empirical treatment before investigations come back - time sensitive
-Bacterial meningitis - ceftriaxone
-Viral encephalitis - aciclovir
Stop treatment if diagnostic investigations come back negative

Routine bloods - NAD
CT brain, MRI brain - swollen hippocampus
EEG - some seizure activity
LP - high lymphocytes => inflammation
Viral PCR - negative
Anti NMDA found - 3wks to get results back

Definitive - immunosuppression => manage neoplasm
Seizure management