The cerebellopontine angle syndrome is a distinct neurological syndrome of deficits that can arise due to the closeness of the cerebellopontine angle to specific cranial nerves. Indications include unilateral hearing loss (85%), speech impediments, disequilibrium, tremors or other loss of motor control. The cerebellopontine angle cistern is a subarachnoid cistern formed by the cerebellopontine angle that lies between the cerebellum and the pons. It is filled with cerebrospinal fluid and is a common site for the growth of acoustic neuromas or schwannomas. Signs and Symptoms
Tumors within the nerve canaliculi initially present with unilateral sensorineural hearing loss, unilateral tinnitus, or disequilibrium (vertigo is rare, on account of the slow growth of neuromas). Speech discrimination out of proportion to hearing loss, difficulty talking on the telephone are frequent accompaniments. Tumors extending into the CPA will likely present with disequilibrium or ataxia depending on the amount of extension on the brainstem. With brainstem extension, midfacial and corneal hypesthesia, hydrocephalus, and other cranial neuropathies become more prevalent. For example, involvement of CN V from a cerebellopontine mass lesion often results in loss of the ipsilateral (same side of the body) corneal reflex (involuntary blink). Patients with larger tumours can develop Bruns nystagmus (dancing eyes) due to compression of the flocculi. Causes
In most cases, the cause of acoustic neuromas is unknown. The only statistically significant risk factor for developing an acoustic neuroma is having a rare genetic condition called neurofibromatosis type 2 (NF2). There are no confirmed environmental risk factors for acoustic neuroma.
Supportive therapy is given if necessary, including respiratory assistance and maintenance of body temperature. Once a person has had a normal ECG for more than 24 hours they are generally medically clear. Decontamination
Initial treatment of an acute overdose includes gastric decontamination. This is achieved by giving activated charcoal, which adsorbs the drug in the gastrointestinal tract either by mouth or via a nasogastric tube. Activated charcoal is most useful if given within 1 to 2 hours of ingestion. Other decontamination methods such as stomach pumps, ipecac induced emesis, or whole bowel irrigation are generally not recommended in TCA poisoning. Stomach pumps may be considered within an hour of ingestion but evidence to support the practice is poor. Medication
Administration of intravenous sodium bicarbonate as an antidote has been shown to be an effective treatment for resolving the metabolic acidosis and cardiovascular complications of TCA poisoning. If sodium bicarbonate therapy fails to improve cardiac symptoms, conventional antidysrhythmic drugs or magnesium can be used to reverse any cardiac abnormalities. However, no benefit has been shown from Class 1 antiarrhythmic drugs; it appears they worsen the sodium channel blockade, slow conduction velocity, and depress contractility and should be avoided in TCA poisoning.