Recurrent obstructive hydrocephalus in a 4-month-old infant.

INTRODUCTION: Transient, recurrent or permanent causes of hydrocephalus in children are usually due to tumours, cerebral bleeding or colloid cysts and complications of infectious meningitis or secondary to poisoning. Recurrent, obstructive hydrocephalus is very rare. CASE REPORT: We report a 4-month-old boy who suffered at least three different episodes of obstructive hydrocephalus presumably caused by intermittent valvular blockage of the normal aqueduct cerebrospinal flow as indirectly demonstrated by serial standard and dynamic brain imaging studies. In addition, he had congenital left hydronephrosis secondary to congenital ureteropelvic junction stenosis. The child underwent an endoscopic third ventriculostomy with only transient post-surgical complications (i.e. central diabetes insipidus). DISCUSSION: The neurological symptoms rapidly improved after surgery, and the child is currently doing well with normal psychomotor development.

Incidence and causes of neonatal hyperbilirubinemia in a center of Catania.

AIM AND SCOPE: We conducted this study to estimate the incidence of hyperbilirubinemia in a small neonatal care unit in Catania, Italy, and to determine the underlying causes, which would be of value in identifying and implementing strategies to prevent morbidity from this condition. BACKGROUND: Management of hyperbilirubinemia remains a challenge for neonatal medicine because of the risk for serious neurological complications related to the toxicity of bilirubin. METHODS: From January 2006 to January 2007, we screened 525 newborns born at the Neonatal Care Unit of Valsalva Hospital in Catania, Italy. Infants aged 3-5 days and with unconjugated hyperbilirubinemia were included for assessment if they had a peak serum total bilirubin level exceeding 6 mg/dl (102 mumol/L). Sex, birth weight, gestational age, breast feeding, type of birth, presence of facial bruising (including cephalohematoma) and ABO group were noted. Patients with Toxoplasma or Cytomegalovirus infection, hepatic insufficiency, or suspected drug-induced hyperbilirubinemia were excluded from more detailed analysis. RESULTS: Our year-long nursery sample examined otherwise healthy-appearing term infants for the prevalence of hyperbilirubinemia (defined as bilirubin levels exceeding 6 mg/dL [11mol/L]). We found hyperbilirubinemia in 19% (100/525). Among the patients with hyperbilirubinemia, almost all (99%) had peak levels of bilirubin <20 mg/dL, levels which are generally considered to be potentially neurotoxic. CONCLUSIONS: In our clinic experience, hyperbilirubinemia was generally a serious medical issue and one whose etiology can usually be well defined.

Effects of L-acetylcarnitine on cirrhotic patients with hepatic coma: randomized double-blind, placebo-controlled trial.

Multiple therapeutic modalities have been used to treat hepatic encephalopathy. L: -Acetylcarnitine (LAC) is a physiologically active substance that improves both the energetic and the neurotransmission profiles. LAC is able to cross the hematoencephalic barrier and reach the cerebral regions, where the acetylic group may be utilized. The aim of this work was to evaluate the efficacy of LAC in the treatment of hepatic coma in cirrhotic patients. Twenty-four suitably selected patients were enrolled in the study and, following randomization, received either LAC (n=13) or placebo (n=11). Statistically significant differences in neurological findings, as evaluated by the Glasgow Scale, as well as in ammonia serum levels and BUN were found following LAC treatment. In the placebo group we observed two cases of improved neurological findings as well as one case of improved EEG grading. In the other group we observed an improvement of neurological findings and of EEG grade in 10 and 8 subjects, respectively. Noteworthily, seven (54%) patients went from grade 4 down to grade 3, and one from grade 4 down to grade 1. The improvement in the neurological picture was evident at between 1 and 4 hr after the end of treatment, remaining until 24 hr after. No side effects were observed in our study series. Our study demonstrates that LAC administration improved neurological and biohumoral symptoms in selective cirrhotic patients with hepatic coma.

New possibilities of treatment for panic attacks in elderly patients: escitalopram versus citalopram.

PURPOSE: Panic attacks may represent additional therapeutic problems in the elderly. The utility of citalopram in panic attacks has been widely investigated. Here, we compare the efficacy and safety of citalopram, with its S-enantiomer escitalopram at half dosage as to citalopram, in elderly patients who have panic attacks. METHODS: This was an open community-based study. Forty patients who have panic attacks, according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria, were enrolled. Fifty percent of the patients were assigned for 8 weeks' treatment with escitalopram, and the remaining 50% were assigned to treatment with citalopram. The primary outcome measure was the weekly rate of panic attacks. The secondary outcome measures were the Hamilton scale for anxiety and depression and the Cooper Disability Scale. Analysis of variance by repeated measures was applied to calculate differences between groups. RESULTS: A similar decrease in weekly rate of panic attacks, in the scores of Hamilton Scale for anxiety and depression and in the Cooper Disability Scale scores, was observed in both groups after 8 weeks, but a significant variation of outcome measures from baseline was observed already after 2 weeks in the escitalopram group (P < 0.001) and only after 4 weeks in the citalopram group (P < 0.01). CONCLUSIONS: Escitalopram could be considered among the drugs of first choice in elderly patients with panic attacks because of its good efficacy and safety and for the advantage of reducing the total dose and of a more rapid onset of action as compared with citalopram, although further studies are needed to confirm these results.

Tic disorders: from pathophysiology to treatment.

Tic disorders are stereotypic behaviours,more frequent than once believed, and therefore likely to be encountered by primary care physicians. Tics usually begin in childhood and are the clinical hallmark of Tourette Syndrome (TS), the most common cause of tics. TS is a relatively common neurobehavioural disorder with a spectrum of manifestations that wax and wane during its natural course. The pathophysiology of tics, at molecular and cellular level, is still unknown,whereas structural and functional neuroimaging studies have shown the involvement of the basal ganglia and related cortico-striato-thalamo-cortical circuits, and the dopaminergic neuronal system. Moreover, TS has a strong genetic background. The management of TS is often complicated by the presence of attention-deficit/hyperactivity disorder, obsessive-compulsive disorder, and other behaviour disorders. The correct diagnosis is a fundamental step for a proper management of these disorders, and a multimodal treatment is usually indicated. This approach includes educational and supportive interventions, as well as pharmacological treatments when tics are at their worst.

Is it safe to use antidepressants after a stroke?

Depression is an important complication of stroke. Although antidepressants are widely used for the treatment of poststroke depression (PSD), prescription is critically influenced by their safety, tolerability and by the impact on co-morbidities. The authors reviewed the literature on the use of antidepressants after stroke. Selective serotonin re-uptake inhibitors are effective and have a good profile of safety and tolerability in PSD. They are, therefore, used as first-line drugs in the treatment of PSD, although potential cardiovascular and cerebrovascular effects, drug-drug interactions and intolerability in a minority of patients have to be considered. Other antidepressants appear to be safe and effective in selected patients. PSD patients should be classified according to their clinical profile for the selection of the drug of choice in particular sub-groups of patients.

An evaluation of efficacy and safety of reboxetine in elderly patients affected by "retarded" post-stroke depression. A random, placebo-controlled study.

Depression occurs frequently in post-stroke patients and appears to be associated with an impairment in their rehabilitation and functional recovery. Although selective serotonin reuptake inhibitors (SSRI) are often used in post-stroke depression (PSD), it has been observed that only a subset of patients is responsive to this treatment. Other patients respond to tricyclic antidepressants or MAO inhibitors, which, however, may not have a favorable profile of safety and tolerability in post-stroke patients. In this double-blinded, placebo-controlled study, we evaluated the efficacy and tolerability of the noradrenaline reuptake inhibitor, reboxetine, in a subset of PSD patients classified as affected by "retarded" depression. Reboxetine (4 mg, twice daily, for 16 weeks) was administered to patients that developed depression after a single ischaemic or hemorrhagic stroke. We assessed the severity of depressive symptoms by the Beck Depression Inventory (BDI) and Hamilton Depression Rating Scale (HDRS). HDRS and BDI scores (mean+/-S.D.) at baseline were, respectively, 24+/-1.31 and 19.87+/-1.46 in the placebo group, 24.06+/-1.52 and 20.56+/-2.16 in the reboxetine group. After 16 weeks, HDRS and BDI mean scores were respectively 22.73+/-2.4 and 18.4+/-3.33 in the placebo group, 9.26+/-2.15 and 8.06+/-3.43 in the reboxetine group [p<0.01 versus the respective baseline (paired t-test); (#)p<0.01 versus retarded depressed patients treated with placebo (one-way analysis of variance (ANOVA) applied to the difference from baseline, associated with Dunnett's t-test to isolate the differences)]. Reboxetine showed a good efficacy, safety and tolerability in PSD patients affected by "retarded" depression. We conclude that reboxetine is well tolerated and may be a useful therapeutic option in PSD patients with "retarded" depression.

Evaluation of the prophylactic efficacy of amitriptyline and citalopram, alone or in combination, in patients with comorbidity of depression, migraine, and tension-type headache.

Antidepressants are used to treat chronic daily headache disorders such as migraine and chronic tension-type headache (TTH), which are often associated with depression and anxiety. Here, we studied the efficacy and tolerability of amitriptyline and citalopram, given alone or in combination, in patients with 'triple' comorbidity of depression, TTH, and migraine. Eighty-eight patients were enrolled in the study and randomly divided into two groups. The first group received amitriptyline and the second citalopram for 16 weeks. Patients were assessed at weeks 0, 4, 8, and 16. The two drugs were equally efficacious in relieving depressive symptoms, although amitriptyline was more efficacious than citalopram in reducing migraine and TTH attacks. Patients who did not respond to monotherapy (<30% of improvement in the clinical scores) were treated with a combination of the two drugs for 16 additional weeks. In these selected patients, the combined treatment produced a substantial improvement in depression, migraine and TTH without producing major side effects such as those commonly related to the 'serotonergic' syndrome. The results indicate that a combined therapy with amitriptyline and citalopram may be particularly beneficial for patients with TTH, migraine and comorbid depression that do not respond to monotherapy.

Blink reflex abnormalities in Tourette syndrome.

OBJECTIVE: Tourette syndrome (TS) is a not uncommon disorder which represents the most complex manifestation of the spectrum of tic disorders, with onset during childhood or early adolescence. There are no definitive tests for diagnosis of TS. The objective of this study has been to demonstrate whether neurophysiological abnormalities of the blink reflex can be observed in patients affected with TS and correlate with the severity of TS. METHODS: We enrolled 17 patients with Tourette syndrome, diagnosed according to DSM IV Diagnostic Criteria, and 10 healthy volunteers. Tic severity was assessed using a self rating scale (Tourette Syndrome Symptom List, TSSL) and examiner ratings (Yale Global Tic Severity Scale (YGTSS), and Tourette-Syndrome Global Scale (TSGS)). The blink reflex was elicited by stimulating the supraorbital nerve in order to measure the early response (R1), homolateral and contralateral R2 (late) responses, amplitude of R1 and duration of R2. RESULTS: We observed a mean duration of R2 significantly longer in the patient group than in the control group (P<0.01, Student t test), without any statistically significant differences of R1 and R2 latencies and of R1 amplitude between the patient group and the control group. Correlations between changes in clinical rating scores and R2 duration were tested by simple linear regression analysis, which has not demonstrated a significant correlation between TSSL scores, clinical rating scores (measured by TSGS and YGTSS) and duration of R2. CONCLUSIONS: A pattern as to excitability of the blink reflex can be a frequent abnormality in TS patients, not correlated with its severity.

Prediction of the response to citalopram and reboxetine in post-stroke depressed patients.

RATIONALE AND OBJECTIVE: Depression is a significant complication of stroke. The effectiveness of antidepressant drugs in the management of post-stroke depression (PSD) has been widely investigated. However, the choice of antidepressant drug is critically influenced by its safety and tolerability and by its effect on concurrent pathologies. Here we investigate the efficacy and safety of a selective serotonin reuptake inhibitor (SSRI), citalopram, and a noradrenaline reuptake inhibitor (NARI), reboxetine, in post-stroke patients affected by anxious depression or retarded depression. METHODS: This was a randomized double-blind study. Seventy-four post-stroke depressed patients were diagnosed as affected by anxious or retarded depression by using a synoptic table. Randomisation was planned so that 50% of the patients in each subgroup were assigned for 16 weeks to treatment with citalopram and the remaining 50% were assigned to treatment with reboxetine. The Beck Depression Inventory (BDI), the Hamilton Depression Rating Scale (HDRS) and a synoptic table were used to score depressive symptoms. RESULTS: Both citalopram and reboxetine showed good safety and tolerability. Citalopram exhibited greater efficacy in anxious depressed patients, while reboxetine was more effective in retarded depressed patients. CONCLUSIONS: Citalopram or other SSRIs and reboxetine may be of first choice treatment in PSD because of their good efficacy and lack of severe side effects. In addition, PSD patients should be classified according to their clinical profile (similarly to patients affected by primary depression) for the selection of SSRIs or reboxetine as drugs of choice in particular subgroups of patients.

Gerstmann-Sträussler-Scheinker disease with P102L-V129 mutation: a case with psychiatric manifestations at onset.

Gerstmann-Sträussler-Scheinker disease (GSS) is an adult onset, rare, genetically determined autosomal dominant prion disease. Clinically, it is characterized predominantly by slowly progressive spino-cerebellar dysfunction with ataxia, absent reflexes in the legs and cognitive impairment. Onset is usually in the fifth decade and in the early phase, ataxia is predominant. Mutations in the prion protein gene (PRNP) had been identified and the most important of these is at codon 129. A genotype-phenotype relationship with genetic polymorphism at residue 129 between methionine and valine has been supposed. We describe a patient with GSS and P102L-V129 mutation in which the onset with prominent psychiatric features characterized by apathy and depression and not with cerebellar sign and the clinical course with seizures, nor observed in P102L-V129 cases, allow us to confirm observations that the GSS caused by the 102 mutation is influenced by the codon 129 polymorphism with a specific genotype-phenotype influence, but probably other additional factors might be considered as background for phenotypic variability.

The SSRI, citalopram, improves bradykinesia in patients with Parkinson's disease treated with L-dopa.

Idiopathic Parkinson's disease (IPD) is characterized by motor signs such as akinesia, rigidity, and often tremor at rest. In addition to these symptoms, depression is a common finding affecting 40% of patients with IPD. This study evaluates the effect of the selective serotonin reuptake inhibitor, citalopram, on motor and nonmotor symptoms of depressed and nondepressed patients with IPD. Forty-six nondemented patients with IPD (24 men, 22 women; mean age 64 +/- 5.3 years; mean +/- SD disease duration, 6.4 +/- 3.2 years; mean +/- SD Hoehn-Yahr stage, 2.8 +/- 1.2) were included in the study. Patients were divided in two subgroups: depressed (n = 18) and nondepressed (n = 28). Citalopram was added in an unblinded manner, starting with 10 mg/d, and, after a week, increased up to 20 mg/d in the depressed subgroup (n = 18) and in half of the nondepressed subgroup (n = 14). Parkinsonian and depressive symptoms were evaluated before and after 1 and 4 months of treatment. Statistical evaluation was made by analysis of variance for repeated measures. Citalopram did not worsen motor performance in IPD, but improved bradykinesia and finger taps after 1 month and 4 months of treatment both in patients with and without depression (p < 0.05 versus baseline). A clear improvement in mood was also observed in 15 of 16 patients with depression. Although case reports indicate that citalopram can potentially worsen the motor symptoms in patients with PD, to date this effect has not been confirmed. Many of the symptoms, typically associated with depression, can be observed in nondepressed patients with IPD, because signs thought to represent depression can be produced by Parkinson's disease. In this study, we observed that when combined with levodopa, citalopram induces an improvement of motor performance, in particular of subscores 23 and 31 of Unified Parkinson's Disease Rating Scale both in depressed and in nondepressed patients with IPD.