What is the long term efficacy of betahistine dihydrochloride on the incidence of vertigo attacks in patients with Meniere’s disease, compared with placebo?
The BEMED trial is a multicentre, double blind, randomised, placebo controlled, three arm, parallel group, phase III, dose defining superiority trial conducted in 14 German tertiary referral centres
Results of this interesting study you can find HERE
Internuclear ophtalmoplegia (INO) results from the damage of the MLF (medial longitudinal fasciculus). The eye on the lesional side can’t adduct during horizontal eye movements. That results in dubble vision when looking contralesionaly. But contruary to III nerve paresis, the eye can adduct during convergence eye movement.
The most frequent cause of INO are stroke and MS.
Here’s an interesting work on INO recording eye movements: LINK
Woman 53yr with symptoms which resembles BPPV history, but not very convincing. Her vertigo started in the morning while she was still in the bed with feeling of sinking. All the time she is dizzy and she can’t move the head neither eyes because it worsens her dizziness; slight instability. She vomited for two times. The same symptoms she had two months ago after yoga exercises and three days after, canalith repositioning maneuver completely resolved her symptoms.
No spont Ny. VHIT is good. But Dix-Hallpike shows downbeating nystagmus which is accompanied with slight vertigo (slightly stronger at the right side).
OK. Let’s check for the central vestibular function.
VNG shows good saccades but smooth pursuit is rather saccadic at both directions more pronounced to the right. But the patient is very drowsy because of Chloropyramine (antihystamine).
I’ve performed Epley (for the right) and demi-Semone.
On the next day she is still dizzy and Dix-Hallpike still shows downbeat nystagmus. Also there’s slight myosis at the right eye.
VNG shows better tracking gains but gain to the right is significantly lower!
Deep-head hanging maneuver and Epley didn’t resolved the downbeat nystagmus (slightly less intense).
Few days later, she is without vertigo and also without any positional nystagmus.
MRI shows arachnoid cyst in the right CPA.
Would you attribute her positional downbeat nystagmus:
– to BPPV (anterior or apogeotropic posterior) or
– to arachnoid cyst in contact with 8th cranial nerve and right cerebellar lobe?
Do you send every positional down-beat nystagmus to MRI?
What’s the significance of asymmetric smooth pursuit gain?
According to Timothy C. Hain asymmetric smooth pursuit gain is because of:
– Acute parietal lobe disorder
– Acute frontal lobe disorder
– Superimposed nystagmus
– Lesion of pontine nuclei
43yr woman noticed few month ago when she listened to the music with earphones that it didn’t sound the same at both sides, she haired worse at the left. In her family hearing problems has father, uncle and aunt. She hasn’t have any balance problems.
Here’s her audiogram: reduced hearing at high frequencies at both sides and little bit worse hearing at law tones on the left. Would you ask for more testing in this patient?
She has gaze evoked nystagmus at both sides (Brun’s nystagmus), and torsional up-beat when fixating up-target.
Reduced VOR gain to the left and 50% paresis of the left labyrinth at caloric test.
Slight dysdiadochokinesia with left hand and finger-to-nose slight dysmetria with first try.
VNG shows saccadic smooth pursuit to the left.
MRI shows big CPA tumor 28x27x35mm
– ipsilesional, large amplitude low frequency, because of geze impairment
– contralesional, small amplitude high frequency, because of vestibular impalance
Progressive Supranuclear Palsy (PSP) or Steele-Richardson-Olszewski Syndrome is neurodegenerative dissorder, characterized by akinetic rigid parkinsonism, dizziness, unsteadiness, slowness, falls, and pseudobulbar dysarthria, and also supranuclear eye movement abnormalities which presented as downward, or upward, or combination gaze palsy.
A discussion of neuropathic disorders encompasses those diseases that affect the neuron’s cell body, or neuronopathies, and those affecting the peripheral process, or peripheral neuropathies. Neuronopathies can be further subdivided into those that affect only the anterior horn cells, or motor neuron disease, and those involving only the sensory neurons, also called sensory neuronopathies or ganglionopathies. Peripheral neuropathies can be broadly subdivided into those that primarily affect myelin, or myelinopathies, and those that affect the axon, or axonopathies.
Here’s a very useful protocol for taking history and exam in 6 key questions: Click on link
Sensory neuronopathies (SNs) are a specific subgroup of peripheral nervous system diseases characterized by primary degeneration of dorsal root ganglia and their projections. Multifocal sensory symptoms often associated to ataxia are the classical features of SN. Several different etiologies have been described for SNs, but immune-mediated damage plays a key role in most cases. SN may herald the onset of some systemic autoimmune diseases, which further emphasizes how important the recognition of SN is in clinical practice. Click on link
Of course BPPV can manifest with DBN also, here’s a review on this topic Link to abstract
Positional nystagmus isn’t always benign; here are some characteristics of Central Paroxysmal Positional Nystagmus (CPPV): CPPN may be ascribed to enhanced responses of the vestibular afferents due to lesions involving the nodulus and uvula. CPPN could be differentiated from benign paroxysmal positional nystagmus by positional nystagmus induced in multiple planes, temporal patterns of nystagmus intensity, and associated neurologic findings suggestive of central pathologies. LINK
62yr woman with instability as main complain, lasting for 7 years, which deteriorated in last two years. She felt down for two times completely conscious. Six months ago she noticed double vision when looking to the right. She has slight headaches in occipital part and she is very forgetful. Paresthesias in extremities and clumsiness with hands. Her MRI is still normal.
gaze evoked Ny, from time to time down beat Ny
her speech is slight dysarthric
Romberg is positive: she falls to the right
cerebellar signs positive: dysmetria on the left
patellar reflexes exaggerated, Achilles reflexes absent
diminished sensitivity in the hands and foots
caloric test absent response at both sides
VHIT: absent vestibulo-ocular reflex at all canals
VNG: no smooth pursuit, saccades with prolonged latency to the right, slight overshoot dysmetria to the right and undershoot dysmetria to the left
For CANVAS patients very caracteristic sign is positive VVOR test: this test is positive due to lack of smooth pursuit and lack of vestibulo-ocular reflex and lack of optokinetic reflex.
At this video there’s obvious Horner sign on the right side.
Caracteristic hystory of slowly progressive instability with clinical signs of cerebellar dysfunction and bilateral vestibulopathy and peripheral neuropathy. More about CANVAS at: link
Patient in late 50thies feels one week slight instability from time to time, and describes it as difficulty walking straight and also has a short vertigo spells (discomfort in the head) when moving head, especially quick turns. Also, he complains to have left-sided tinnitus (pulsating hissing) since this instability problems has started. He had no nausea or other symptoms.
This history doesn’t sound like a vestibular neuritis.
He had no spontaneous Ny and head-impulse test was normal, but Fukuda step test showed marked turning to the right.
VHIT showed normal gains in all canals expect left posterior, where gain was markedly reduced. cVEMP showed vestibulo-infraocular reflex bilaterally but significantly lower amplitude at the left side.
Caloric test was normal, no asymmetry at all and audiometry showed bilateral mild hearing loss at high frequencies.
VHIT (6 canals) and cVEMP allowed us to diagnose acute lesion of inferior vestibular nerve branch in this patient. Link with interesting videos of pt with inferior vestibular neuritis, showing spontaneous torsional nystagmus and positive head impulse test in the plane of the affected posterior canal.