Presentation on theme: "Andy and Rick. PC 56 y.o. male w. severe stabbing pains in the R. side of face. HPC Appeared ~6mths ago. ↑ in frequency. Lasts only a few secs. Occurs."— Presentation transcript:
PC 56 y.o. male w. severe stabbing pains in the R. side of face. HPC Appeared ~6mths ago. ↑ in frequency. Lasts only a few secs. Occurs several times a day Triggers – shaving, drinking, eating, windy days Recent wt. loss Dentist found no tooth-related issues Ex Neuro exam finds no abnormalities EXCEPT when the face was tested for touch and pain (?) sensibility, triggered an attack each time R. cheek was touched
DDX (wrong) Dental pian (poor dentist?) Temporal arteritis Cluster headache Maxillary sinusitis TMJ dysfunction Up-to-date DDx Short-lasting unilateral neuralgiform headache w. conjunctival injection and tearing (SUNCT) Cluster tic syndrome Jabs and jolts syndrome ‘Other’ neuralgias (Postherpatic, Provisional Dx Trigeminal Neuralgia Many potential causes of this
In short; there is insufficient evidence to support or refute the utility of MRI to identify neurovascular compression in classic TN, or to indicate the most reliable MRI technique But…. Neuroimaging with head CT or MRI is useful for identifying the small proportion of patients who have a structural lesion (eg, tumor in the cerebellopontine angle, demyelinating lesions including multiple sclerosis) as the cause of secondary TN. In addition, high resolution MRI and magnetic resonance angiography (MRA) may be useful for identifying vascular compression as the etiology of classic TN, but the utility of these studies has not been established. It is suggested to obtain brain MRI for patients in the following groups to rule out a causative structural brain lesion: Patients with trigeminal sensory loss Patients with bilateral symptoms Young patients (under the age of 40)
carbamazepine controlled-release 100 mg orally, once or twice daily; increase as tolerated and according to response every 7 days up to a maximum of 600 mg twice daily. After pain relief has been maintained for several weeks, the dose should be gradually reduced to establish the minimum dose that will provide good pain control. If carbamazepine is ineffective, options include referral to a neurosurgeon or trial of other drugs alone or in combination with carbamazepine. Murtagh suggests these as options for alternative drug therapy: Gabapentin Phenytoin Clonazepam Baclofen Surgery Possible procedures include: Decompression of the trigeminal nerve root (eg. Gel foam packing between the nerve and blood vessels Thermocoagulation/radiofrequency neurolysis Surgical division of the peripheral branches
THE REST OF THIS DOC IS A GOOD CONCISE SUMMARY OF TRIGEMINAL NEURALGIA FROM MURTAGHS
Trigeminal neuralgia (tic douloureux) is a condition of often unknown cause that typically occurs in patients over the age of 50, affecting the second and third divisions of the trigeminal nerve and on the same side of the face. Brief paroxysms of pain, often with associated trigger points, are a feature.
Site: sensory branches of the trigeminal nerve almost always unilateral (often right side) Radiation: tends to commence in the mandibular division and spreads to the maxillary division and (rarely) to the ophthalmic division Quality: excruciating, searing jabs of pain like a burning knife or electric shock Frequency: variable and no regular pattern Duration: 1 - 2 minutes (up to 15 minutes) Onset: spontaneous or trigger point stimulus Offset: spontaneous Precipitating factors: talking, chewing, touching trigger areas on face (e.g. washing, shaving, eating), cold weather or wind, turning onto pillow Aggravating factors: trigger points usually in the upper and lower lip, nasolabial fold or upper eyelid Relieving factors: nil Associated features: rarely occurs at night spontaneous remissions for months or years Signs: there are no signs, normal corneal reflex Causes: unknown local pressure on the nerve root entry zone by tortuous pulsatile dilated small vessels (probably up to 75%) multiple sclerosis neurosyphilis tumours of the posterior fossa Note: Precise diagnosis is essential.
Patient education, reassurance and empathic support is very important in these patients. Medical therapy: carbamazepine (from onset of the attack to resolution)4 50 mg (elderly patient) or 100 mg (o) bd initially, gradually increase the dose to avoid drowsiness every 4 days to 200 mg bd (maintenance); testing serum levels is unnecessary; higher dosage may be necessary alternative drugs if carbamazepine not tolerated or ineffective (but question the diagnosis if lack of response) gabapentin 300 mg daily initially, then increase phenytoin 300 - 500 mg daily clonazepam baclofen Surgery: refer to a neurosurgeon if medication ineffective possible procedures include: decompression of the trigeminal nerve root (e.g. gel foam packing between the nerve and blood vessels) thermocoagulation/radiofrequency neurolysis surgical division of peripheral branches