INVESTIGATION

MRI of the brainstem and spinal cord:

Should be considered in all patients and usually undertaken if;

The presentation is acute or rapidly progressive
There are predominantly sensory symptoms (including back pain).
There is predominant sphincter disturbance at presenatation.
There is a very distinct or obvious sensory or motor level.

To rule out a cause of structural myelopathy (e.g. haemorrhage or tumour) which may rarely present as a flaccid paraparesis.

Lumbar Puncture:

Elevated CSF protein without pleocytosis is a supportive diagnostic finding. However the CSF may be normal within seven days of onset of symptoms.[3]

Protein level - elevated after the first week of symptoms.
WCC - < 10/mm3, occasionally up to 50/mm3
Glucose level - normal

Neurophysiology:

Normal nerve conduction studies in the first week do not exclude the diagnosis of Guillain-Barre Syndrome.
May be useful in children who present with atypical features, normal CSF protein after the first week following presentation or in categorising the subtype of GBS e.g. Acute Motor Axonal Neuropathey (AMAN).[6,15,16]

Other Investigations:

FBC, blood culture (if pyrexial).
U&E (hypokalaemia).
CXR, ECG.
Abdominal Xray (palpable bladder, constipation).

To identify an underlying cause:

Acute and convalescent serum for viral and mycoplasma antibody titres (Mycoplasma pneumoniae, EBV, CMV, Borrelia burgdorferi).
Throat swab; stool C&S (Campylobacter jejuni).
Antiganglioside antibodies (e.g anti-GQ1b antibodies in Miller-Fischer).

The following investigations should be considered if a secure diagnosis is not confirmed.

Heavy metals and toxins ( lead, mercury, arsenic, organophosphates)
Urinary porphyrins
Botulinum toxin identification (stool, serum)
Drug toxicology screen

Miscellaneous:

If investigations have been normal or negative (MRI, CSF analysis, eletrolytes), consideration should be given to a trial of

i.v. edrophonium (Tensilon) and/or
Oral pyridostigmine (minimum of five days)

for a myasthania syndrome