Trigeminal Electrophysiology: a 2 × 2 matrix model for differential diagnosis between temporomandibular disorders and orofacial pain

Background Pain due to temporomandibular disorders (TMDs) often has the same clinical symptoms and signs as other types of orofacial pain (OP). The possible presence of serious neurological and/or systemic organic pathologies makes differential diagnosis difficult, especially in early disease stages. In the present study, we performed a qualitative and quantitative electrophysiological evaluation of the neuromuscular responses of the trigeminal nervous system. Using the jaw jerk reflex (JJ) and the motor evoked potentials of the trigeminal roots (bR-MEPs) tests, we investigated the functional and organic responses of healthy subjects (control group) and patients with TMD symptoms (TMD group). Method Thirty-three patients with temporomandibular disorder (TMD) symptoms and 36 control subjects underwent two electromyographic (EMG) tests: the jaw jerk reflex test and the motor evoked potentials of the trigeminal roots test using bilateral electrical transcranial stimulation. The mean, standard deviation, median, minimum, and maximum values were computed for the EMG absolute values. The ratio between the EMG values obtained on each side was always computed with the reference side as the numerator. For the TMD group, this side was identified as the painful side (pain side), while for the control group this was taken as the non-preferred masticatory side (non-preferred side). The 5th, 10th, 25th, 50th, 75th, 90th, and 95th percentiles were also calculated. Results Analysis of the ratios (expressed as percentages) between the values obtained on both sides revealed a high degree of symmetry in the bR-MEPs % in the control (0.93 ± 0.12%) and TMD (0.91 ± 0.22%) groups. This symmetry indicated organic integrity of the trigeminal root motor fibers and correct electrode arrangement. A degree of asymmetry of the jaw jerk's amplitude between sides (ipJJ%), when the mandible was kept in the intercuspal position, was found in the TMD group (0.24% ± 0.14%) with a statistically significant difference in relation to the control group (0.61% ± 0.2%). This asymmetry seemed to be primarily due to a failure to facilitate the reflex on the painful side in intercuspal position. Conclusions In this 2 × 2 matrix diagnostic model, three different types of headache may be identified: 1) those due to organic pathologies directly and indirectly involving the trigeminal nervous system denoted as "Organic Damage"; 2) those in TMD patients; 3) other types of orofacial pain in subjects who could erroneously be considered healthy, denoted as Orofacial Pain "OP". This category of patient should be considered at risk, as organic neurological pathologies could be present and yet not directly affect the trigeminal system, at least in the early stages of the disease.</p

A Relationship between bruxism and orofacial-dystonia? A trigeminal electrophysiological approach in a case report of pineal cavernoma

Background: In some clinical cases, bruxism may be correlated to central nervous system hyperexcitability, suggesting that bruxism may represent a subclinical form of dystonia. To examine this hypothesis, we performed an electrophysiological evaluation of the excitability of the trigeminal nervous system in a patient affected by pineal cavernoma with pain symptoms in the orofacial region and pronounced bruxism. Methods: Electrophysiological studies included bilateral electrical transcranial stimulation of the trigeminal roots, analysis of the jaw jerk reflex, recovery cycle of masseter inhibitory reflex, and a magnetic resonance imaging study of the brain. Results: The neuromuscular responses of the left- and right-side bilateral trigeminal motor potentials showed a high degree of symmetry in latency (1.92 ms and 1.96 ms, respectively) and amplitude (11 mV and 11.4 mV, respectively), whereas the jaw jerk reflex amplitude of the right and left masseters was 5.1 mV and 8.9 mV, respectively. The test stimulus for the recovery cycle of masseter inhibitory reflex evoked both silent periods at an interstimulus interval of 150 ms. The duration of the second silent period evoked by the test stimulus was 61 ms and 54 ms on the right and left masseters, respectively, which was greater than that evoked by the conditioning stimulus (39 ms and 35 ms, respectively). Conclusions: We found evidence of activation and peripheral sensitization of the nociceptive fibers, the primary and secondary nociceptive neurons in the central nervous system, and the endogenous pain control systems (including both the inhibitory and facilitatory processes), in the tested subject. These data suggest that bruxism and central orofacial pain can coexist, but are two independent symptoms, which may explain why numerous experimental and clinical studies fail to reach unequivocal conclusions.</br

P2‐477: IMPROVING THE HEALTHCARE OF PEOPLE WITH DEMENTIA: A MODEL FOR DEMENTIA CARE PATHWAY FROM THE "CARLO POMA" HOSPITAL (ITALY)

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Heme biosynthesis in human breast cancer-mimetic "in vitro" studies and some heme enzymic activity levels

1. 1. Porphyrin biosynthesis from 5-aminoevulinic acid (ALA) was investigated using the technique of tissue explant cultures, in both human breast cancer and its original normal tissue. 2. 2. The activity of ALA-dehydratase, porphobilinogenase and uroporphyrinogen decarboxylase was directly determined in both tumor and normal mammary tissues. 3. 3. Porphyrin synthesis capacity of human breast carcinoma was 20-fold enhanced, as compared with normal tissue, at least between the stages of porphobilinogen and coproporphyrinogen formation. 4. 4. The activity of the three enzymes examined was always lower in normal tissue than in tumoral tissue. 5. 5. Present findings show that porphyrin biosynthesis is increased in breast cancer tissue. © 1990

Gamification in Late-Life Depression: A Serious Game for a Serious Problem

In the older population, one of the serious health concerns associated with negative outcomes such as comorbidity, loss of physical autonomy, excessive use of health care resources, and increased mortality is the onset of mood disorder [1]. Late-life depression (LLD) is an umbrella term to define depressed mood in people older than 65 years. It can have a variety of presentations: as recurrent disease stemming from earlier life (early onset depression [EOD]); as new-onset depression (late-onset depression [LOD]); as a mood disorder secondary to a general medical condition; or as mood symptoms secondary to substance or medication use [2]. Mistakenly, LLD is believed as a normal part of aging. For older people, depression could be the epiphenomenon of underlying biological processes (vascular changes, metabolic disturbances and neurodegenerative diseases); conversely, it could be the leading cause of cognitive impairment [3]

Neuropsychiatric Symptoms, Endophenotypes, and Syndromes in Late-Onset Alzheimer's Disease: Focus on APOE Gene

Neuropsychiatric symptoms, previously denominated as behavioural and psychological symptoms of dementia, are common features of Alzheimer's disease (AD) and are one of the major risk factors for institutionalization. At present, the role of the apolipoprotein E (APOE) gene in the development of neuropsychiatric symptoms in AD patients is unclear. In this paper, we summarized the findings of the studies of neuropsychiatric symptoms and neuropsychiatric syndromes/endophenotypes in AD in relation to APOE genotypes, with special attention to the possible underlying mechanisms. While some studies failed to find a significant association between APOE and neuropsychiatric symptoms in late-onset AD, other studies reported a significant association between the APOE ε4 allele and an increase in agitation/aggression, hallucinations, delusions, and late-life depression or anxiety. Furthermore, some negative studies that focused on the distribution of APOE genotypes between AD patients with or without neuropsychiatric symptoms further emphasized the importance of subgrouping neuropsychiatric symptoms in distinct neuropsychiatric syndromes. Explanations for the variable findings in the existing studies included differences in patient populations, differences in the assessment of neuropsychiatric symptomatology, and possible lack of statistical power to detect associations in the negative studies

effectiveness of switching therapy from complexing protein containing botulinum toxin type a to a formulation with low immunogenicity in spasticity after stroke a case report

Objective: some patients receiving botulinum toxin type a therapy develop immunological resistance due to the production of neutralizing antibodies against the neurotoxin, thus partially or completely reducing the therapeutic effect. Case report: We report here neurophysiological and clinical findings for a 58-year-old man treated with botulinum toxin type A for spasticity after ischaemic stroke, who became a secondary non-responder patient. subsequent treatment with a different preparation of botulinum toxin type A had a great therapeutic effect on his spasticity. the muscles injected and the dosages were the same for each treatment, but evaluation with the Modified Ashworth Scale after treatment with the second preparation showed a reduction of approximately 2 points compared with the first examination. The clinical results were also supported by extensor digitorum brevis testing of the right muscle, which showed a reduction in compound muscle action potential, whereas it was unchanged in the non-injected muscle. No side-effects were reported, and after 1 year of treatment with this formulation clinical benefits were still evident. Conclusion: the neurophysiological and clinical results obtained in this patient suggest that switching therapy from a complexing protein-containing product to a product potentially free of complexing proteins, which has low immunogenicity, may be a viable therapeutic option in secondary non-responder patients