confusing patient case

[lazymarket99]

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So I helped see a patient in clinic the other day (I'm an MS3), and was a little confused, hoping somebody would help me out. My attending kinda brushed me off when I asked for an explanation.

Patient is a young male in 20s w/ h/o HIE a few mths ago, presenting for evaluation of "unsteady walking". Cognitively functional. He was in coma w/ ICU stay for ~ 1 wk. He is taking some psych meds (low dose ssris/low dose lithium) with h/o antipsychotic use for a week a month ago. On PE, he has significantly decreased cadence and stride length in his gait. When he attempts to run, he is completely uncoordinated and does not have appropriate gait. Mild fine tremor in hands that waxes and wanes. Significant shaking of BLE when touching his toes or attempting to increase stride length of gait. He does not fall on romberg, but is definitely shaky. Most confusing though, his foot actually is very unsteady (shifting around in place) when he steps, and is exacerbated when he attempts to hold a unilateral flexed hip position. He can not plantarflex past 90 deg. Strength was 4+/5 on BLE/BUE. all other PE (cerebellar) was normal. MRI Brain showed occipital and L ant frontal brain infarcts.

So my confusion is why does the patient have significant unsteadiness (major complaint)? My attending said it was due to HIE, but that doesn't make sense to me since cerebellum was ok, along with motor strip. I assume decreased cadence/stride length is secondary to unsteadiness. Proprioception is abnormal but doesn't seem to be in line with the unsteadiness. I would think that the leg shaking would be due to weakness from deconditioning, but strength is 4+/5. My best guess would be at least partially related to poor plantarflexion? Idk, I'm very confused by this case.

Tks for your help...I know this is a long post!

 

[MerickManual]

What was his HIE due to? Any TBI? Any spasticity? How is his ROM? Reflexes? Any clonus? Any h/o PT/OT in the past, how did he walk after his HIE/ICU stay? Kind of hard to really tell you anything, your description of his gait is very vague.

 

[TUGM]

any nystagmus or vestibular abnormalities? any trauma that could have injured his lumbar plexus?

 

[warchild]

the basal ganglia are particularly sensitive to hypoxic-ischemic encephalopathy and damage can result in a range of movement disorders, from akinetic-rigid syndrome, to dystonia, to chorea, tics, delayed parkinsonism etc. Imaging findings in the basal ganglia secondary to hypoxia can be very subtle.

 

[neurodoc]

I note that he is on lithium and has a tremor. In order to determine whether or not his motor problems are due to
HIE, you would have to see how he does when he's off his meds. There is a somewhat rare and apparently idiosyncratic
condition, lithium related cortical myoclonus, that can produce exactly the kind of symptoms you describe. I was recently
consulted by a psychiatrist colleague whose patient was on lithium and who had a pretty bad myoclonic tremor. I thought
that the patient was "toxic" on his lithium, but it turned out that his lithium level was "low normal." We held the lithium and
the symptoms resolved. In this particular case the lithium was clearly helping the patient, so it was restarted at a very low
dose. The patient did well on the lower dose but developed disabling motor side effects with any attempts to achieve
"normal" lithium levels. It turned out that the patient seemed to do OK (psychiatrically) with lithium levels just below the
"normal" range.

 

[thumper2]

If the movement looks like myoclonus, look into an entity called Lance-Adams syndrome, which is a post-hypoxic movement disorder characterized by action-induced myoclonus. Even if this isn't what your patient has, it's an interesting disorder to be aware of.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309367/