Botulinum Toxin Type A in Dental Medicine.

Botulinum toxins (BoNTs) are a product of the bacteria Clostridium botulinum. By entering nerve endings, they cleave and inactivate SNARE proteins, which are essential for neurotransmitter release. Prevention of acetylcholine release at the neuromuscular junction causes long-lasting and potentially fatal flaccid paralysis-a major feature of botulism. However, an intramuscular injection of minute amounts of BoNTs, primarily type A (BoNT-A), has useful long-lasting muscle relaxation effects on spastic motor disorders. This characteristic of BoNT-A is widely used in neurology and cosmetics. Over the last few decades, it has been demonstrated that the functions of BoNT-A are not limited to muscle-relaxing or autonomic cholinergic effects but that it can act as an analgesic agent as well. More recently, it was revealed that this antinociceptive effect starts after entering the sensory nerve endings, where these agents are axonally transported to the central nervous system, suggesting that at least part of their analgesic effect might be of central origin. Because of its antinociceptive effect, BoNT-A is currently approved for treatment of chronic migraine; nonetheless, case reports and preclinical and clinical experiments indicating its benefit in numerous potential painful conditions have increased. In the field of dentistry, the US Food and Drug Administration approved BoNT-A for the treatment of sialorrhea only. Legal status of the use of BoNT-A in other countries is less known. However, there are controlled clinical trials suggesting its efficacy in other conditions, such as bruxism, temporomandibular disorders, and trigeminal neuropathic pain. Thereby, using criteria of the American Academy of Neurology, we critically reviewed the uses of BoNTs in oral medicine and found it effective for trigeminal neuralgia (category A) and probably effective in temporomandibular disorders and bruxism.

Incidence of seizures with tricyclic and tetracyclic antidepressants.

One hundred eighty-six depressed psychiatric inpatients were seen at our institution during 1982. Forty-five of these patients were treated with tricyclic antidepressants, 32 received maprotiline hydrochloride, a tetracyclic compound, 20 received other medications, and 82 received no drug treatment. One patient in the tricyclic group (2.2%) and five patients in the maprotiline group (15.6%) developed seizures. In four patients the seizure followed the institution of maprotiline therapy by less than three weeks. These data indicate that depressed patients taking the tetracyclic drug maprotiline are at risk for developing epileptic seizures.

Peripheral dystonia.

We studied four patients with distal, action-induced involuntary postures of the hand that could be considered focal dystonia. All four patients had electrophysiologic findings consistent with peripheral nervous system lesions (pronator teres syndrome, radial nerve palsy, lower brachial plexus lesion, or median nerve lesion). With varying success, patients were treated with carbamazepine, trihexyphenidyl, methocarbamol, and wrist splinting. We wish to emphasize that peripheral entrapment and brachial plexopathy should be added to the causes of secondary dystonias.

Predicting posttraumatic epilepsy in penetrating head injury.

Using data derived from a 15-year follow-up study of 520 veterans surviving penetrating brain wounds received in the Vietnam war, we have developed a predictive formula and tables for posttraumatic epilepsy based on time elapsed postinjury and presence of specific clinical and computed tomographic scan risk factors. Such patients remain at some increased risk for epilepsy even ten to 15 years postinjury, although most can be 95% certain of avoiding epilepsy if they have been seizure free for three years posttrauma. Epilepsy onset latency was independent of any risk factors identified.

The value of visual evoked potential as a screening test in neurofibromatosis.

Pattern reversal visual evoked potential (VEP) test was performed in 30 asymptomatic patients with neurofibromatosis (NF). All patients had normal visual acuity, visual fields, and ophthalmoscopic examination results. Pattern reversal VEP was abnormal in eight patients (26%). Seven of these patients had computed tomographic scans with reformated orbital views. Orbital computed tomographic scans were abnormal in six patients and in each case showed enlargement of the optic nerve on the side of VEP abnormality. Our data indicate that pattern reversal VEP is a valuable screening test in asymptomatic patients with NF. Because of the high incidence of VEP abnormality in such patients, VEP abnormality must be interpreted cautiously when a patient with NF is suspected of having other diseases or disorders that potentially affect the visual pathways.

Magnetic resonance imaging in partial complex epilepsy.

The yield of magnetic resonance (MR) imaging was investigated in 30 patients with partial complex epilepsy, and the results were compared with those of computed tomography (CT). Magnetic resonance imaging and CT disclosed focal cerebral abnormalities in 13 (43%) and eight (26%) patients, respectively. Two additional focal temporal lesions were identified by double-dose CT scanning, increasing the yield of CT to 33%. Magnetic resonance images were abnormal in all patients with focally abnormal CT scans, and in four patients (50%) they defined the extent of the temporolimbic lesions better than did the CT scans. Two of these patients had gliomas. In addition, MR images were focally abnormal in 85% of the patients in whom scalp electroencephalograms showed focal ictal discharges. These data indicate that MR imaging is more informative than CT in partial complex epilepsy.

EEG, transmission computed tomography, and positron emission tomography with fluorodeoxyglucose 18F. Their use in adults with gliomas.

We evaluated the relationship between findings from EEG, transmission computed tomography (CT), and positron emission tomography in 23 adults with gliomas. The cortical metabolic rate was suppressed in patients with and without focal slowing. Focal delta activity was not related to involvement of gray or white matter. Rhythmic delta activity and focal attenuation of background amplitude on EEG, however, were correlated with involvement of the thalamus.

Miosis and internal ophthalmoplegia as a manifestation of partial seizures.

We present a patient whose only physical manifestation of a partial sensory seizure was bilateral pupillary constriction and internal ophthalmoplegia. The onset and offset of each attack corresponded distinctly with an electroencephalographic discharge of the left temporo-occipital region. We propose involvement of a cortical pupillary constrictive center in the temporal-occipital area.

Concurrent cerebral venous sinus thrombosis and myeloradiculopathy in Sjögren's syndrome.

A 41-year-old woman complained of severe headaches and developed quadriparesis and neurogenic bladder. Evaluation disclosed the presence of Sjögren's syndrome complicated by myeloradiculopathy with MRI evidence of cervical cord involvement. Concurrent cerebral venous sinus thrombosis was also noted. Treatment with steroids and warfarin led to clinical improvement and resolution of MRI findings.

Spinal cord compression due to pseudomonas in a heroin addict. Case report.

Involvement of the spinal cord has not been reported in osteomyelitis of the spinal column caused by Pseudomonas aeruginosa. Cerebrospinal fluid findings have been reported only once in osteomyelitis of the spine by this agent. Our patient had persistently increased cerebrospinal fluid protein during an acute episode of cervical spine osteomyelitis, characterized by fever and neck pain. Roentgenograms of the cervical spine and neurologic examination did not show any definite abnormality. He became paraplegic 18 months later, after having symptoms of numbness of the feet and progressive weakness of the legs for 1 month. A surgical procedure and antibiotic treatment resulted in remarkable recovery. A bone specimen grew P. aeruginosa.

Paroxysmal, rhythmic lingual movements and chronic epilepsy.

Paroxysmal and rhythmic lingual movements were observed in three children during a study designed to investigate epileptiform movements of oropharyngeal muscles in patients with chronic epilepsy. The movements were confined to the tongue, occurred mainly during sleep, and were observed again in two children 7 and 18 months later. These movements corresponded to episodic desynchronization of the electroencephalogram and were attributed to an unusual form of subcortical seizures.

Botulinum toxin A and chronic low back pain: a randomized, double-blind study.

OBJECTIVES: To investigate the efficacy of botulinum toxin A in chronic low back pain and associated disabilities. METHODS: Thirty-one consecutive patients with chronic low back pain who met the inclusion criteria were studied: 15 received 200 units of botulinum toxin type A, 40 units/site at five lumbar paravertebral levels on the side of maximum discomfort, and 16 received normal saline. Each patient's baseline level of pain and degree of disability was documented using the visual analogue scale (VAS) and the Oswestry Low Back Pain Questionnaire (OLBPQ). The authors reevaluated the patients at 3 and 8 weeks (visual analogue scale) and at 8 weeks (OLBPQ). RESULTS: At 3 weeks, 11 of 15 patients who received botulinum toxin (73.3%) had >50% pain relief vs four of 16 (25%) in the saline group (p = 0.012). At 8 weeks, nine of 15 (60%) in the botulinum toxin group and two of 16 (12.5%) in the saline group had relief (p = 0.009). Repeat OLBPQ at 8 weeks showed improvement in 10 of 15 (66.7%) in the botulinum toxin group vs three of 16 (18.8%) in the saline group (p = 0.011). No patient experienced side effects. CONCLUSION: Paravertebral administration of botulinum toxin A in patients with chronic low back pain relieved pain and improved function at 3 and 8 weeks after treatment.

Botulinum toxin A for spasticity, muscle spasms, and rigidity.

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.

Improvement of ataxic hemiparesis with trihexyphenidyl.

In a patient with the syndrome of crural paresis and homolateral ataxia, administration of trihexyphenidyl resulted in improvement of disabling unilateral ataxia and gross intention tremor. Symptoms returned when drug therapy was interrupted. CT showed a radiolucent lesion deep in the parietal white matter close to the internal capsule.

Computed tomography in a verified case of tuberculous meningitis.

In a verified case of tuberculous meningitis, postcontrast computed tomograms demonstrated enhancement of the area corresponding to the cistern surrounding the brainstem. This enhancement disappeared after successful drug treatment of the meningitis.

Nifedipine for intractable hiccups.

Seven patients with intractable hiccups were treated with a calcium channel blocker, nifedipine. A daily dose of 30 to 60 mg of this drug stopped hiccups in 4 patients and improved them in a 5th patient. In 2 patients hiccups recurred within 24 hours after stopping nifedipine. Nifedipine can be effective against intractable hiccups in some patients.

Nerve agents: a review.

Nerve agents produce neuromuscular blockade and convulsions in exposed humans. Military personnel in areas of potential exposure take prophylactic pyridostigmine. They are instructed to self-administer atropine and pralidoxime at the first sign of nerve agent toxicity. The key to treatment of nerve agent poisoning is the administration of atropine in doses larger than is customary in most other disorders, repeated as often as needed. Mechanical ventilation may be required. Convulsions are treated with diazepam, but only after atropine has been administered.

Early abnormalities of brainstem auditory evoked potentials in Friedreich's ataxia: evidence of primary brainstem dysfunction.

We studied five children with classic Friedreich's ataxia, using an audiologic test battery to determine the primary site of auditory dysfunction. None of the children had any hearing complaints, and all were tested soon after onset of symptoms. The audiologic test battery consisted of brainstem auditory evoked potential test, tympanometry, and acoustic reflex measurements. The results indicated that the brainstem was the primary site of auditory dysfunction.

Contrast agent overdose causing brain retention of contrast, seizures and parkinsonism.

A patient received an overdose of intravascular contrast medium and experienced protracted seizures associated with radiographic evidence of prolonged retention of the contrast agent in the cerebral cortex, basal ganglia, and thalami. This is only the second report and the first survivor of a similar neurologic syndrome occurring in a patient after contrast agent overdose. After the seizures resolved, there was a transient period of parkinsonism probably due to the toxic effect of contrast on the basal ganglia.

Epilepsy after penetrating head injury. I. Clinical correlates: a report of the Vietnam Head Injury Study.

Of 421 veterans who had penetrating brain wounds in Vietnam 15 years ago, 53% had posttraumatic epilepsy, and one-half of those still had seizures 15 years after injury. The relative risk of developing epilepsy dropped from about 580 times higher than the general age-matched population in the first year to 25 times higher after 10 years. Patients with focal neurologic signs or large lesions had increased risk of epilepsy, and site of the lesion may have been more important than size in determining occurrence. Family history of epilepsy or preinjury intelligence had no effect on seizure occurrence. Seizure frequency in the first year predicted future severity of seizures. Phenytoin therapy in the first year after injury did not prevent later seizures.