Vertigo, hearing loss, weak legs and dyskinesia Flashcards Preview

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Flashcards in Vertigo, hearing loss, weak legs and dyskinesia Deck (27):

Vertigo - is this vertigo?

  • Definition – an illusion of movement, often rotatory of the patient or his surroundings. In practice patients say ‘I veer sideways on walking’. Vertigo is always worsened by movement.
  • Associated symptoms – difficulty walking or standing, relief on lying or sitting still, nausea, vomiting, pallor or sweating. Hearing loss or tinnitus implies VIIIth cranial nerve involvement.
  • Symptoms not related to vertigo - faintness – may be due to anxiety with associated palpitations, tremor and sweating. Light-headedness – anaemia, orthostatic hypotension or effort in emphysema. Loss of awareness – during attacks suggests epilepsy or syncope.


Vertigo - causes

Usually the labyrinth, vestibular nerve or vestibular nuclei is involved.

  • Labyrinth or VIIIth nerve problem – Meniere’s disease, acute labyrinthitis, benign positional vertigo, motion sickness, trauma, ototoxic drugs or zoster (in Ramsey Hunt syndrome).
  • Brainstem, cerebellum, cerebello-pontine angle – look for nystagmus and cranial nerve lesions -  caused by MS, stroke or TIA, haemorrhage, migraine or acoustic neuroma.
  • Others – vertiginous epilepsy or alcohol intoxication.


Vertigo - benign positional vertigo

Due to canaloilithiasis – debris in the semicircular canal is disturbed by head movement and resettles causing vertigo that lasts a few seconds after the movements (often caused by turning over in bed).

Diagnosis is made by nystagmus on performing the Hallpike manoeuvre and debris can be cleared from the semicircular canals by the Epley manoeuvre


Vertigo - acute labyrinthitis

Abrupt onset of severe vertigo, nausea and vomiting ± collapse but there is no deafness or tinnitus. Vertigo subsides in days and a complete recovery takes place over 3-4 weeks.


Vertigo - Menieres disease

Aka endolymphatic hydrops causes recurrent attacks of vertigo lasting >20 minutes (± nausea and vomiting), fluctuating sensorineural hearing loss (may be permanent) and tinnitus. Drop attacks may rarely occur – no loss of consciousness or vertigo but sudden falling to one side. 

Management – acute attacks can be treated with bed rest and antihistamine e.g. cinnarizine if prolonged or buccal prochlorperazine if severe for up to 7 days.


Vertigo - ototoxicity

Aminoglycosides, loop diuretics or cisplatin can cause deafness ± vertigo.


Vertigo - acoustic neuroma

Doubly misnamed as it is a schwannoma arising from the vestibular nerve. It often presents with unilateral hearing loss with vertigo occurring later.

With progression ipsilateral Vth, VIth, IXth and Xth nerves may be affected and cerebellar signs may occur. Signs of raised ICP occur much later and suggest the presence of a large tumour. More common in women and in neurofibromatosis type 2.


Vertigo - traumatic damage

Involving the petrous temporal bone or the cerebellar pontine angle often affects the auditory nerve causing vertigo, deafness ± tinnitus.


Hearing - testing

Use a 512Hz tuning fork struck a third from its free end on your patella.

  • Weber’s test – place fork in the centre of the forehead. Ask where the sound is loudest – in normal patients this should be in the middle or equally in both ears. If louder in one ear – either conductive deafness in this ear or sensorineural deafness in other ear.
  • Rinne’s test – hold fork next to external auditory meatus then place it on the mastoid process. Ask whether it is louder in front of or behind the ear. In normal patients air conduction should be better than bone conduction (AC > BC) and the test is positive. If test is negative (BC > AC) then this suggests a conductive deafness in the affected ear.


Hearing - conductive deafness

Caused by wax, otosclerosis, otitis media or glue ear.


Hearing - sensorineural deafness

  • Chronic sensorineural deafness – often due to accumulated environmental noise toxicity, presbyacusis or inherited disorders. Presbyacusis is loss of acuity for high frequency sounds which starts before 30 years but is not usually noticed until hearing of speech is affected.
  • Sudden sensorineural deafness – get an urgent ENT opinion – causes include noise exposure, gentamicin, mumps, acoustic neuroma, multiple sclerosis, stroke, vasculitis or TB.


Hearing - tinnitus definition

Ringing or buzzing in the ears is common and may cause depression or insomnia. The mean age of onset is between 40-50 years of age and men and women are equally affected. Tinnitus should always be investigated when unilateral to exclude acoustic neuroma as a cause.


Hearing - tinnitus causes

Focal hyper-excitability in the auditory cortex, hearing loss, wax, viral infection, Presbyacusis, excess noise (e.g. gunfire), head injury, septic otitis media, post stapedectomy, Meniere’s disease, anaemia, hypertension or drugs – aspirin, loop diuretic or aminoglycosides.

  • Causes of pulsatile tinnitus – carotid artery stenosis or dissection or an arteriovenous fistula - needs an MRI


Hearing - tinnitus management

Psychological support from a hearing therapist, tinnitus coping training and patient support groups can help greatly.

Drugs are disappointing – avoid tranquilisers, but hypnotics may help and give tricyclic antidepressants if depressed.

Masking may give some relief – white noise is delivered via a noise generator worn like a post-aural hearing aid. 


Cord compression - questions

Typically presents with leg weakness – there are 6 questions to ask:

  • Was the onset gradual or sudden?
  • At what rate is the weakness progressing?
  • Are the legs spastic or flaccid?
  • Is there sensory loss (a sensory level usually means spinal cord disease)?
  • Is there loss of sphincter control (e.g. bowel or bladder)?
  • Are there any signs of infection (spine tenderness or raised WCC)?


Cord compression - progressive weakness

Rapidly progressing cord compression is a medical emergency – hours make a difference as untreated irreversible loss of power and sensation below the level of the lesion and a neurogenic bladder and bowel will develop.


Cord compression - symptoms and signs

  • Symptoms – spinal or root pain may precede leg weakness and sensory loss. Arm weakness is often less severe and suggests a cervical spinal cord lesion. Bladder (and anal) sphincter involvement is a late sign and manifests as hesitancy, frequency and painless retention. 
  • Signs – look for normal neurological findings above the level of the lesion and upper motor neurone signs below the level of the lesion.


Cord compression - causes

Secondary malignancy (breast, lung, prostate, thyroid and kidney) in the spine is the most common cause.

Rarer causes are infection (epidural abscess), cervical disc prolapse, haematoma (in patients on warfarin), intrinsic cord tumour, atlanto-axial subluxation or myeloma.


Cord compression - investigations

Never delay a spinal MRI and biopsy or surgical exploration may be needed to identify the nature of any mass.

Screening blood tests – FBC, ESR, vitamin B12, folate, syphilis serology, Us and Es, LFTs, PSA and serum electrophoresis.

Do a CXR – to look for malignancy, lung secondaries and TB.


Cord compression - management

If caused by malignancy give 4mg IV dexamethasone QDS whilst considering more specific treatment e.g. radiotherapy or chemotherapy ± decompressive laminectomy.

An epidural abscess must be surgically decompressed and antibiotics must be given.


Cord compression - paralysed patients care

Avoid pressure sores by turning the patient, check weight bearing areas often, avoid thrombosis in paralysed limbs by frequent passive movement, pressure stockings ± low molecular weight heparin.

Bladder care is vital e.g. with catheterisation and bowel evacuation may be manual or aided by suppositories - increasing dietary fibre may also help.


Dyskinesia - tremor

Note the frequency, amplitude and exacerbating factors e.g. stress or fatigue

  • Resting tremor – abolished on voluntary movement – caused by parkinsonism.
  • Intention tremor – irregular, large amplitude worse at the end of purposeful action e.g. finger pointing or using the remote control. Causes cerebellar damage – by stroke or MS.
  • Postural tremor – absent at rest and present on maintained posture e.g. arms outstretched. Causes – benign essential tremor (improves with EtOH), thyrotoxicosis, anxiety or β blockers.
  • Re-emergent tremor – a postural tremor developing after 10 secs delay – in parkinsonism.


Dyskinesia - chorea

Non-rhythmic, jerky purposeless movements flitting from one place to another e.g. facial grimacing, raising the shoulders and flexing and extending of the fingers.

Causes – Huntingdon’s disease and Sydenham’s chorea (a rare complication of Strep infection – rheumatic fever).


Dyskinesia - hemiballismus

Large amplitude, flinging hemichorea (affects proximal muscle) contralateral to a vascular lesion of the subthalamic nucleus (in elderly diabetics) – recovers spontaneously in months.


Dyskinesia - athetosis and pseudoathetosis

Athetosis - slow, sinuous, confluent purposeless movements (especially the digits, hands, face and tongue) often difficult to distinguish from chorea - usually caused by cerebral palsy.

Pseudoathetosis - caused by a severe proprioceptive impairment.


Dyskinesia - myoclonus

Sudden involuntary focal or general jerks arising from the cord, brainstem or cerebral cortex. Found in metabolic problems, neurodegenerative disease, CJD or myoclonic epilepsies.

  • Benign essential myoclonus – childhood onset with frequent generalised myoclonus without progression. It is often autosomal dominant and may respond to valproate or clonazepam.
  • Asterixis – ‘metabolic flap’ – jerking of outstretched hands, worse with the wrists extended, from loss of extensor tone. Causes – hepatic or renal failure, hyponatraemia or CO2 retention.


Dyskinesia - tardive syndromes

Tardive means delayed onset, e.g. after chronic exposure to dopamine antagonists e.g. antipsychotics or antiemetic’s. May be permanent despite discontinuing all drugs.

Examples include tardive dyskinesia (chewing or grimacing movements), tardive dystonia, tardive akathisia, tardive myoclonus or tardive tourettism or tardive tremor.

Management of tardive dyskinesia – gradually withdraw neuroleptics a wait 3-6 months – if dyskinesia is still a problem give tetrabenazine. Quetiapine and clozapine are less likely to cause side effects.