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BMJ Case Rep. 2010; 2010: bcr10.2009.2380.
Published online 2010 January 13. doi:  10.1136/bcr.10.2009.2380
PMCID: PMC3028420
Reminder of important clinical lesson

Post-traumatic dizziness

Abstract

Following an episode of syncope, a 42-year-old woman was referred to exclude a cardiac cause. This primary event was determined to be a straightforward case of vasovagal syncope, resulting in mild head trauma. Following this, the patient was left with symptoms of dizziness and a subjective “muzzy” sensation. Initially assumed to be a form of “post-concussive symptom”, she was referred to a neurologist who employed neurovestibular manoeuvres to both determine the cause of these symptoms and satisfactorily resolve them.

Background

Dizziness is an extremely common symptom after head trauma and is frequently dismissed as post-concussion syndrome. However, when symptoms occur in episodes of brief duration and are related to movement of the head, clinicians should consider a diagnosis of benign paroxysmal positional vertigo (BPPV). Specific neurological examination can diagnose this condition and importantly vestibular manoeuvres exist that can correct this disabling and under-recognised disorder.

Case presentation

A 42-year-old previously fit and well woman suffered an episode of syncope in the early hours of the morning. She fell backwards and struck the occipital region of her head. Although making an instant recovery of consciousness, she found that on two occasions when she tried to get up off the floor she fell back again. Several minutes later she recovered sufficiently to get to her feet with support from her husband. At this point she noticed bleeding at the point where she had struck her head and that a swelling was developing on the back of her head. She attended a local accident and emergency department where a superficial laceration and contusion were noted and she was discharged home.

Seven days after the head trauma she continued to experience episodes of vertigo, lasting 10–20 s, triggered by looking up or down and by turning over in bed. There was no past history of note or of similar dizziness. She was a non-smoker with modest alcohol intake and no significant past medical history.

Cardiovascular examination was unremarkable, with a regular pulse of 70/min, a blood pressure of 130/70 mm Hg, no postural drop, and normal heart sounds. Neurological examination was normal apart from rotational nystagmus, triggered by a modified Dix-Hallpike manoeuvre to the left.

Investigations

The resting 12 lead electrocardiogram showed sinus rhythm at 68/min, a normal axis, morphology and cardiac intervals. A 24 h Holter monitor demonstrated sinus rhythm throughout, with a normal diurnal variation in heart rate. A computed tomographic (CT) scan of the brain revealed only extracranial soft tissue swelling at the site of trauma and no intracerebral abnormality.

Differential diagnosis

A diagnosis of benign paroxysmal positional vertigo (BPPV) arising from the left posterior semicircular canal was made on the basis of the history and clinical examination. As a note of caution, the presence of other neurological signs or symptoms including headache, hearing loss and photophobia should prompt exclusion of other causes. Given the history of head trauma, it is particularly important to consider a structural lesion; it may be appropriate to request a CT scan of the head with skull windows. The full differential diagnosis of recurrent dizziness is extensive, but might include Meniere’s disease, migraine, cerebrovascular events or, as was initially suspected in our case, a cardiac rhythm disturbance.

Treatment

A therapeutic Semont manoeuvre was performed in outpatients. Within a week many of the symptoms had resolved. An Epley manoeuvre was then performed with the patient feeling 90% better a week later.

Details of both the diagnostic (Dix–Hallpike) and therapeutic (Semont and Epley) manoeuvres are beyond the scope of this report and are recently described in a review of BPPV management.1 Both therapeutic manoeuvres are designed to encourage debris (otoconia) to migrate from the posterior semicircular canal back into the utricle. Some patients may be suitable to undertake home exercises (Brandt–Daroff exercises) for posterior semicircular canal BPPV. Other manoeuvres are available when the horizontal and anterior semicircular canals are found to be responsible. These procedures need to be performed by an experienced clinician able to interpret the character and direction of the provoked nystagmus to the particular semicircular canal. Only with correct interpretation can the appropriate therapeutic manoeuvre be applied.

Outcome and follow-up

Following the Epley manoeuvre, the patient was discharged and on telephone follow-up a month later her symptoms had completely settled.

Discussion

These symptoms are characteristic of BPPV, with neurological examination indicating involvement of the left posterior semicircular canal.

Recurring short episodes of vertigo following trauma are not uncommon. In BPPV the symptoms of pseudo rotation of the environment occur on movement of the head in certain positions. Post-traumatically, tiny fragments of debris (otoconia), in fluid of the inner ear semicircular canals, are caused to move about. Otoconia are made up of calcium carbonate crystals that arise from within the utricle, a fluid filled chamber forming part of the labyrinth. If the head is struck, otoconia particles may be jettisoned and become free floating (canalithiasis) in the semicircular canals. With movement of the head, these fragments are swept along in the fluid and brush against hairs that line the semicircular canals to create a false sense of motion. The result to the patient is a sensation of vertigo. Clinically, this is apparent as nystagmus after a characteristic latency of a few seconds, with rapid resolution (usually 20–30 s) once the head is still.

When idiopathic in origin, BPPV usually occurs in older people and is more common in women than men. As in our case, the posterior semicircular canal is affected in 85–95% of cases, probably in relation to its position at the lowest point, where the otoconia are likely to collect.2 We have shown that the diagnosis can be confirmed by manoeuvres consisting of controlled movement of the patient’s head in the plane of the semicircular canal thought to be responsible.

An understanding of these vestibular rehabilitation techniques has now resulted in drug therapies being considered largely inappropriate in this condition.3

Learning points

  • Benign paroxysmal positional vertigo (BPPV) is a common and treatable condition that is frequently missed.
  • BPPV is a common sequelae to significant head trauma, but can also occur after mild trauma, which accounts for around 18% of cases.4
  • BPPV is diagnosed using the Dix–Hallpike manoeuvre.
  • BPPV is amenable to therapies using one of several restorative vestibular manoeuvres.

Footnotes

Competing interests: None.

Patient consent: Patient/guardian consent was obtained for publication.

REFERENCES

1. Management of benign paroxysmal positional vertigo. Drug Ther Bull 2009; 47: 62–6. [PubMed]
2. Battacharyya N, Baugh RF, Orvidas L, et al. Clinical practice guideline: benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 2008; 139(5 Suppl 4): s47–81. [PubMed]
3. Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2008; 70: 2067–74. [PubMed]
4. Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987; 37: 371–8. [PubMed]

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