The differential diagnosis for multiple infarcts in multiple vascular distributions
#1 embolism
#2 coagulopathy
#3 vasculitis
#4 all the rest
Primary CNS vasculitis is also called granulomatous angiitis
Respiratory patterns and critical illness
Cheynes Stokes -diffuse forebrain pathology
central neurogenic hyperventilation- midbrain and upper pons
apneustic - tegmentum
cluster breathing - tegmentum and lower pons
ataxic -reticular activating and dorsomedial medulla
Differential diagnosis of a large fiber neuropathy that spares the small fibers
Sjogren's
B12 deficiency
CIDP
multifocal motor neuropathy with delayed conduction
Small fiber distal symmetric neuropathy differential diagnosis
diabetes
heavy-metal poisoning
amyloid -classic for small fiber neuropathy
paraneoplastic
hematologic
inherited
idiopathic
Patient has a positive finding on a monoclonal study, you need to consider fat aspirate and refer to hematology
Diagnostic tests for small fiber neuropathies can normally be made clinically if all you have is tingling and burning. However consider a qSART, thermoregulatory sweat test. Key points to ask in history are autonomic symptoms bowel bladder dysfunction sexual dysfunction and orthostatic hypotension. Parkinson's and multiple systems atrophy can often present with complete hypohidrosis.
Indications for a sural nerve biopsy:
suspected sarcoidosis without any other good biopsy site
leprosy
vasculitis
amyloid
unexplained neuropathy
Approach to the patient with dementia. Key questions to sort out in the history.
Is this a dementia?
Is this reversible?
In the history TIA history of stroke?
Sleep history
who is doing the finances, has the patient ever gotten lost, as the patient lost the ability to drive, does the patient have obstructive sleep apnea, has the patient's sense of smell changed?
Keep in mind many causes of dementia are overlapping for example Lewy body dementia and vasculitis or Alzheimer's disease and vasculitis
early short-term memory loss is a clue for Alzheimer's. First to changes are in the entorhinal cortex and then progress to the hippocampus to the medial temporal lobe and then to the frontal lobe.
Lewy body dementia
presenting with a dementia then the synucleinopathy is in the cortex
presenting with parkinsonism than the synucleinopathy is in the substantia nigra
REM sleep disorders come from lesions in the peduncular pontine nuclei
REM sleep disorder, new data show a 50% chance of progression to dementia and 15 years from the onset of their REM sleep disorder, 82% at 25 years
anti MA–1 anti-voltage gated potassium channel anti-bodies are also associated with REM sleep behavior disorder
Quick notes on chronic pain meds
alpha lipoic acid has been used successfully in painful diabetic neuropathy
acetyl l-carnitine has also been used for painful diabetic neuropathy
for any given agent patient has to be on it for a few weeks to make a clinical judgment as to whether it works.
The big mistake with tricyclic antidepressants and painful neuropathy is that the dose is too low. Increased doses are usually done with extreme caution because of the anticholinergic side effects. This usually prevents finding an adequate dose.
Duloxetine – 60 mg daily for paying 60 mg twice daily to double cover psychiatric disease.
Side effects while described hyperhidrosis withdrawal and increases bleeding risk with patients on warfarin
Gabapentin big side effect is swelling dizziness and sedation. You can increase the dose but be aware that the G.I. transporters saturate at around 2000 mg daily. This is not seen with pregabalin because it's effective at a much lower dose.
Topiramate -for chronic pain should be working at doses between 200 to 400 mg daily. Lower doses are usually seen with migraine prophylaxis. Major side effects include renal stones and paresthesias and cognitive cloudiness.\
Lamotrigine- normally avoided because of risk of Stevens-Johnson syndrome. Active doses around 200 400 mg per day six-week titration to minimize the risk of Stevens-Johnson syndrome.
When treating pain start with level I which is to treat the cause topical agents gabapentin pregabalin TCAs and duloxetine
level II – anti-epileptics specifically the sodium channel blockers and the SNR eyes such as venlafaxine
Level III opioids and other interventions such as tens units intrathecal pumps
Subscribe to:
Posts (Atom)
