Increased platelet activation has been suggested as a possible reason for the increased vulnerability of depressed patients to ischemic heart disease (IHD). Translocation of P-selectin, an integral alpha-granule membrane protein, to the platelet surface is a measure of platelet activation. Herein, western blots of platelet plasma membranes containing P-selectin were quantified in patients with major depression (n=19; mean age=39 +/- 2 years) and healthy comparison subjects (n=17; mean age=36 +/- 2 years). None evidenced clinical signs of IHD, and only two patients had a lifestyle IHD risk factor (smoking). Blood was obtained from all 19 depressed patients before treatment, and 15 returned after 6-8 weeks of open-label bupropion treatment. Bupropion was chosen as the antidepressant because it did not elevate plasma norepinephrine or serotonin, endogenous agonists that can induce platelet degranulation. Western blotting revealed more P-selectin immunoreactivity (75 kD band) in depressed patients compared to healthy controls (P=0.003). After bupropion treatment, P-selectin remained high in depressed patients. beta3-Integrin, a reference plasma membrane protein that does not translocate during activation, was of equivalent density in depressed patients and healthy control subjects, and was unchanged after treatment with bupropion. P-Selectin failed to correlate with severity of illness based on the Hamilton Depression scale, or with the post-treatment plasma concentration of bupropion. The results suggest an elevation in P-selectin on platelet plasma membranes might be a trait marker for depression.

Adolescent↗

PubMedDate not supplied

Effect of bupropion on immunodensity of putative imidazoline receptors on platelets of depressed patients.

A substantial number of studies have demonstrated increased imidazoline receptors (I1 binding sites) on platelets of depressed patients and downregulation following antidepressant treatments. Herein, imidazoline receptor binding protein (IRBP) antiserum was used to quantify imidazoline receptors on platelets of depressed patients before and after treatment with the atypical aminoketone antidepressant, bupropion. Western blots revealed an increase in IRBP-immunodensity (p = 0.01, two-tailed) in a 33 kDa protein band in untreated depressed patients (n = 21) as compared with controls (n = 17). This band has been positively correlated with I1 binding sites on platelets. Following 6 weeks' treatment with bupropion, IRBP-immunodensity was downregulated in depressed patients (p = 0.03, paired t-test); predominantly in responders (p = 0.005). Patients non-responsive to bupropion (n = 5) were significantly different from responders (p = 0.05) by exhibiting no elevation in IRBP-immunodensity at pre-treatment and no downregulation of the 33 kDa band after treatment. IRBP-immunodensity was negatively correlated (r = -0.79, p = 0.01) with plasma concentrations of bupropion and its metabolites at week-4 of BUP treatment. Thus, a 33-kDa IRBP on platelet plasma membranes is elevated in depression and normalized in responders to bupropion.

Adolescent↗

PubMedDate not supplied

Epilepsy presenting as memory disturbances.

Six patients presented with severe adult-onset memory deficit that was subsequently diagnosed as complex partial epilepsy. In three cases acute amnestic episodes also occurred. The seizures were characterized by short losses of contact and oral automatisms. Interictal EEG showed temporal abnormalities of varying degrees. Formal neuropsychological assessment revealed dissociation between the subjective complaint and the test performances that showed a selective impairment in a few long-term verbal memory tests. These patients present a characteristic clinical picture of memory disturbance as the prominent feature of partial seizures.

Adult↗

PubMedDate not supplied

[Acquired aphasia with convulsion anomalies in the developmental age: clinical neuropsychological and electroencephalographic study of a case].

A four year old boy presented three epileptic seizures of psychomotor type; immediately after he began to show a progressive and rapid dissolution of speech, until he became completely aphasic after few weeks. Since then, repeated EEG examinations have always shown anomalies of epileptic type, located on the left hemisphere, at times on the right, at times bilaterally asynchronous. The neurological, psychic, audiological, chemical-biological and neuro-radiological (bi-lateral carotidogram and penumoencephalogram) exams did not show any other anomalies. After an observation period three years, the AA. underline the following evolutive aspects of the case: 1) The aphasic syndrome is on the way to slow improvement both in its expressive component and in its perceptive component. The recovery of speech seems to follow, with a slower rhythm, the stages of acquisition of the speech in the normal subject. 2) Diversely from other cases of the literature, no positive correlation exists between the gravity of the aphasic syndrome and that of the EEG anomaly: they have worsened while the disturbance of the speech have partially regressed.

Age Factors↗

PubMedDate not supplied