[Chronic facial pain from psychiatric point of view - differential diagnosis and therapeutic strategies]. / Gesichtsschmerzen in der Psychiatrie Differenzialdiagnosen und therapeutische Empfehlungen.

Chronic facial pain may cause diagnostic and therapeutic difficulties, thus demanding a complete interdisciplinary consultation. As in 20 to 25% of patients with a nociceptive or primary neuropathic pain a psychiatric comorbidity is expected, it is necessary to include psychiatric and psychosomatic examinations. Every 8th male and every 4th female pain patient has the statistical risk of having a depression at the same time. Depression may develop as a consequence of pain, but may also be the primary basis for a pain syndrome. An independent coincidence is possible as well. Besides affective disorders, persistent somatoform pain syndromes, syndromes of conversion, hypochondriac or artificial disorders and pain in psychosis have to be excluded in patients presenting with chronic facial pain. In depression, persistent somatoform pain syndromes, atypical facial pain but also when dysfunctional illness beliefs and coping mechanisms are present, cognitive-behavioral therapy should be offered to the patient. Motivation to psychotherapy may be difficult, especially in patients relying exclusively on physical illness beliefs. The physician should develop and extend the physical illness beliefs together with the patient to a model that includes biological as well as psychosocial factors. Tricyclic antidepressants may be indicated not only in depression, but also in chronic pain due to the analgetic effects of these drugs. The choice of drug therapy should conform to the main complaints of depression and accompanying illnesses. Indication of antidepressants or neuroleptic drugs in somatoform pain syndromes is still unclear. Their potential slight effect may simply be due to the high comorbidity between somatoform pain syndromes and depression.

Manifestation of Hashimoto's encephalopathy years before onset of thyroid disease.

Patients with Hashimoto's encephalopathy (HE), a steroid-responsive disorder, associated with Hashimoto's disease and high levels of thyroid-related autoantibodies usually present with a subacute onset of confusion, focal or generalized seizures. Frequent EEG abnormalities include generalized, rhythmic bifrontal or temporal slowing. Elevated protein levels or an intrathecal IgG synthesis may be present in cerebrospinal fluid (CSF). A 39-year-old woman underwent a relapsing course of myocloni and generalized seizures. Initially, thyroid function, thyroid-related autoantibody screening and cerebral MRI were unrevealing. CSF showed oligoclonal bands. Short-term treatment with high doses of prednisolone resolved the myocloni. During the 5th episode of myocloni, signs of hyperthyroidism and elevation of thyroid microsomal antibody titer developed. Hashimoto's thyroiditis and HE were diagnosed. After subtotal thyroidectomy the patient remained asymptomatic.