by Dr Linxin Li, Dr Aubretia McColl, and Dr Robert Hurford

Transient isolated brainstem symptoms are commonly seen in patients with definite posterior circulation stroke.1 However, not all patients with transient isolated brainstem syndromes are having TIAs.

Today in your TIA clinic, there is a 79-year-old gentleman, with previous history of untreated hypertension, diabetes, hyperlipidaemia and migraine with visual aura. He presented with a 3-week history of episodic rotational vertigo and a muzzy head.

What else would you want to know from the history?

Yes, you would want to know how it started.  It all started one day when he stood back upright after washing his face. He had a sudden onset of rotational vertigo, felt nauseated and was unsteady. He also felt his right ear was “full” and he could not hear from his right ear. There was no tinnitus. Overnight, the vertigo settled but he was left with a ‘muzzy head’ (“like a hangover”). He continued to have occasional attacks of vertigo and the ‘muzzy head’ persisted.

Anything else you might want to know?

Yes, we would want to know if there is any trigger for each episode. He said it was worse whenever he stood up.

On examination, he was in sinus rhythm. Blood pressure 151/86mmHg with no postural drop.

What are the differentials on your list?  Will you do an MRI?

We performed MRI which did not show any restricted diffusion or small vessel disease. However, there was thickening and hyperaemia of the dura both on T2-weighted and post-contrast T1-weighted images suggesting spontaneous intracranial hypotension.

So this is the diagnosis! This could have been easily missed if it had not been for our neuroradiology colleagues.

Although intracranial hypotension is normally presented with orthostatic headache, patients can also present with non-headache manifestations, such as hearing loss, labyrinthine dysfunction – a “Ménière-like” presentation2,  which is caused by the pressure change in the inner ear. Perilymph and cerebrospinal fluid (CSF) communicate freely through a patent cochlear aqueduct. Therefore a decrease in CSF pressure (e.g. from a dural leak) can cause a decrease in perilymphatic pressure. Endolymphatic pressure volume changes are however much slower. As a result, endolymphatic pressure exceeds perilymphatic pressure, and both the vestibular and basilar membranes are distorted, causing disruption to the hair cell function.3

So, take home message: spontaneous intracranial hypotension can also present to a TIA clinic and always look outside the brain itself when reading a MRI scan!

 

  1. NLM Paul, M Simoni, PM Rothwell. Transient isolated brainstem symptoms preceding posterior circulation stroke: a population-based study. Lancet Neurol. 2013; 12: 65-71
  2. AA Capizzano, L Lai, J Kim, et al. Atypical presentations of intracranial hypotension: comparison with classic spontaneous intracranial hypotension. Am J Neuroradiol. 2016; 37:1256-1261
  3. N Fontaine, A Charpiot, C Debry, et al. A case of spontaneous intracranial hypotension: from Meniere-like syndrome to cerebral involvement. Eur Ann Otorhinolaryngol Head Neck Dis.2012; 129:153-6.