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Biomedical subjects

M Iivanainen

Publications and source records attributed to M Iivanainen.

At least 19 recordsLinked to original sources
PubMed2001

Suicide mortality in mental retardation:a 35-year follow-up study.

OBJECTIVE: We investigated suicide mortality among people with mental retardation (MR) over a period of 35 years. METHOD: The nationwide, population-based cohort of 2369 people with MR was followed-up from a representative sample of 9.4% of the population in Finland in 1962. The standardized mortality ratio of suicides was calculated and case studies of all MR suicides based on all available data were performed. RESULTS: Women with MR had an equal suicide risk to Finnish women in general, while men had only one-third of the population risk. Risk factors for suicide were similar to those in the general population. Most suicide victims had mild MR and were hospitalized for comorbid mental disorders. Suicide methods were passive and alcohol was involved in only one case. CONCLUSION: Suicide mortality in MR is significantly lowered among males. Suicide prevention in MR should be focused on people with comorbid mental disorders. Problems in adjustment to new circumstances need to be recognized. Appropriate and adequate treatment of comorbid depression is emphasized.

Adult↗
PubMed2001

Cause-specific mortality of people with intellectual disability in a population-based, 35-year follow-up study.

The aim of the present study was to investigate cause-specific mortality in people with intellectual disability (ID). It was based on a 35-year follow-up study of a nation-wide population of 2369 subjects aged between 2 and 97 years. The 1095 deceased people had accumulated 64 539 person-years. The research took the form of a prospective cohort study with mortality follow-up. Observed and expected deaths were calculated as standardized mortality ratios using the Finnish general population as the reference. Cause-specific mortality ratios were calculated by the level of ID, sex and age. The three most common causes of death were cardiovascular diseases, respiratory diseases and neoplasms. Disease mortality was high up to 40 years of age, but did not increase thereafter. The difference between sexes in cause-specific mortality was smaller than in the general population. Cause-specific mortality differed significantly from the general population, with reduced mortality from neoplasms and external causes, but ageing individuals with mild ID had similar mortality patterns to the general population. The disparities in the cause-specific mortality between younger people with ID and the general population fade with advancing age, producing similar health risks. In preventative work, special attention should focus on common diseases and accidents in the community.

Adolescent↗
PubMed2001

Cancer incidence among people with intellectual disability.

The aim of the present study was to address the unresolved question of the risk of neoplasms among people with intellectual disability (ID). A total of 2173 individuals with ID from a large, representative, nation-wide population study conducted in Finland in 1962 were followed-up for cancer incidence between 1967 and 1997. Standardized incidence ratios (SIRs) were defined as ratios of observed to expected numbers of cancer cases. Expected rates were based on national incidence rates. The observed number of cancers in the cohort (173) was close to what was expected [SIR = 0.9, 95% confidence interval (95% CI) = 0.8-1.0]. There was a significantly reduced risk of cancers of the prostate (SIR = 0.2, 95% CI = 0.0-0.5), urinary tract (SIR = 0.3, 95% CI = 0.1-0.7) and lung (SIR = 0.6, 95% CI = 0.4-1.0). The risk was increased in cancers of the gallbladder (SIR = 2.8, 95% CI = 1.1-5.8) and thyroid gland (SIR = 2.1, 95% CI = 1.0-4.8). The risks of lung and gallbladder cancer were lowest and highest, respectively, in those subjects with profound and severe ID, a group who also had significantly elevated SIRs for brain cancer (SIR = 3.46, 95% CI = 1.5-14.4) and testicular cancer (SIR = 9.9, 95% CI = 1.2-35.6). The incidence of cancer among people with ID was comparable with the general population, despite their low prevalence of smoking and apparently decreased diagnostic screening activity. Nevertheless, a few types of cancer carry a higher risk in the population with ID, possibly because of conditions typical among this group, such as gallstones or oesophageal reflux.

Adolescent↗
PubMed2000

Life expectancy of people with intellectual disability: a 35-year follow-up study.

A 35-year follow-up study based on a nation-wide population study of the life expectancy of people with intellectual disability (ID) was undertaken. The study population consisted of a total of 60,969 person-years. A prospective cohort study with mortality follow-up for 35 years was used and the life expectancy of people with ID was calculated for different levels of intelligence. Proportional hazard models were used to assess the influence of level of intelligence and associated disorders on survival. People with mild ID did not have poorer life expectancy than the general population and subjects with mild ID did not have lower life expectancy in the first 3 decades of life. In cases with profound ID, the proportion of expected life lost was > 20% for almost all age groups. The female preponderance was manifested from the age of 60 years onwards, 25 years later than in the general population. Respectively, survival between sexes differed less. Epilepsy and/or hearing impairment increased the relative risk of death for all levels of ID. The prevalence of people with ID over 40 years was 0.4%. People with ID now live longer than previously expected, and the ageing of people with mild ID appears to be equal to that of the general population, posing new challenges to health care professionals.

Adolescent↗
PubMed1998

Multiple sclerosis: in situ evidence for antibody- and complement-mediated demyelination.

We describe a case of multiple sclerosis characterized by deposition of immunoglobulin and complement in the areas of active demyelination. This was particularly evident for the C9neo antigen, which is a marker for the activated lytic complement complex and was exclusively deposited in the areas of active myelin destruction. In addition, macrophages in the lesions contained degradation products that were immunoreactive for myelin antigens, immunoglobulins, and C9neo antigen. Destruction of myelin sheaths was associated with incomplete loss of oligodendrocytes in the active areas and reappearance of oligodendrocytes with remyelination in the inactive plaque center.

Biomarkers↗
PubMed1998

Circulating leptin has saturable transport into intrathecal space in humans.

BACKGROUND: Leptin is an adipocyte-derived hormone that is thought to provide a negative feedback signal to control body fat mass by interacting with its hypothalamic receptor. The present study was undertaken to examine the uptake of leptin in cerebrospinal fluid (CSF) space in humans and whether the transport of leptin into CSF space is an active phenomenon or due to free access through the blood-CSF barrier. METHODS: We determined serum and CSF leptin concentrations by radioimmunoassay in 17 men [42 +/- 4 years, mean +/- SE; body mass index (BMI) 27.3 +/- 1.8 kg m-2] and 22 women (40 +/- 3 years, BMI 25.1 +/- 1.0 kg m-2). The function of the blood-CSF barrier was evaluated by determining the CSF/serum albumin ratio. RESULTS: Serum leptin concentration was lower in male (5.8 +/- 1.6 microgram L-1) than in female subjects (13.1 +/- 1.7 microgram L-1, P = 0. 001), whereas the concentrations of leptin in CSF were virtually identical in male (0.34 +/- 0.03 microgram L-1) and female (0.36 +/- 0. 03 microgram L-1) subjects. Serum leptin was correlated positively with BMI both in men (r = 0.89, P < 0.01, n = 10) and in women (r = 0.61, P < 0.05, n = 14), whereas no correlation between CSF leptin concentration and BMI was found in either group. The CSF/serum leptin ratio correlated negatively with serum leptin concentration both in men (r = -0.93, P < 0.001) and in women (r = -0.77, P < 0. 001) and with BMI both in men (r = -0.75, P = 0.02, n = 10) and in women (r = -0.64, P < 0.02, n = 14). The CSF/serum albumin ratio was not correlated with the CSF/serum leptin ratio in either group. CSF leptin concentrations and the CSF/serum leptin ratio were virtually identical in subjects with impaired and normal blood-CSF barrier function. CONCLUSION: Thus, our data support the presence of a saturable and active transporter of leptin from circulation into intrathecal space.

Adipose Tissue↗
PubMed1998

Use of antiepileptic drugs in the treatment of epilepsy in people with intellectual disability.

The main principles of antiepileptic drug treatment of epilepsy in patients with intellectual disability are basically the same as for other patients with epilepsy. However, some specific issues need to be taken into account These are primarily associated with the diagnostic difficulties of epilepsy in this population. In addition, a number of other relevant issues, including the degree and location of brain lesion, the nature of the underlying disease, the higher frequency of difficult-to-treat epilepsies, the additional intellectual impairment caused by inappropriate antiepileptic medication, or by frequent and prolonged seizures, the appropriate use of monotherapy versus rational polytherapy, and the use of broad-spectrum antiepileptic drugs will be discussed in the present paper. Although the goals of treatment are to keep the patient seizure-free and alert while preventing possible mental deterioration, we have to accept compromises between these primary goals in many cases. Some people with epilepsy and intellectual disability are very vulnerable to insidious neurotoxic effects; for example, sedative effects caused by phenobarbital, or cognitive and/or cerebellar dysfunction caused by long-term phenytoin, especially together with other drugs. Because of the adverse effects of phenobarbital and phenytoin, these drugs are no longer recommended as a first-choice drugs when long-term antiepileptic medication is required. In primary generalized tonic-clonic seizures, valproate, oxcarbazepine/carbamazepine and lamotrigine are recommended in this order of preference. The corresponding recommendations are: in typical absences, valproate, ethosuximide and lamotrigine; in atypical absences, valproate and lamotrigine; in juvenile myoclonic epilepsy, valproate, lamotrigine and clobazam; in infantile spasms vigabatrin, ACTH and valproate; in Lennox-Gastaut syndrome, valproate, lamotrigine and vigabatrin; in atonic seizures, valproate and lamotrigine; in simple and complex partial seizures with or without secondary generalization, oxcarbazepine/carbamazepine, valproate/ vigabatrin and lamotrigine; and in status epilepticus lorazepam, diazepam and clonazepam together with phenytoin or fosphenytoin. In cases of poor response to the monotherapy recommended above, the following combinations may be indicated: in primary generalized tonic-clonic epilepsy, valproate and oxcarbazepine/ carbamazepine, or valproate and lamotrigine; in typical absences, valproate and lamotrigine, or valproate and ethosuximide; in juvenile myolonic epilepsy, valproate and lamotrigine, or valproate and clonazepam; and in partial epilepsies, add to the monotherapy one of the following drugs, vigabatrin, lamotrigine, gabapentin, tiagabine, topiramate, zonisamide or clobazam. So far, the order of preference of these new drugs remains undetermined. More data are needed on the efficacy and adverse effects of the new drugs based on controlled studies on patients with intellectual disability and epilepsy.

Anticonvulsants↗
PubMed1998

Phenytoin: effective but insidious therapy for epilepsy in people with intellectual disability.

Phenytoin (5,5-diphenylhydantoin), which has been in use for 60 years, is still an important antiepileptic drug. Its primary mechanism of action is modulation of the sustained repetitive firing of neurones by direct inhibition and blockage of voltage-gated sodium channels in the neuronal cell membrane, and by delay of cellular reactivation. The plasma protein binding of phenytoin is normally between 90% and 95%. The drug is rapidly distributed from the blood to the tissues and is almost completely metabolized in the liver. The plasma phenytoin concentration normally reaches the steady-state level within 1-2 weeks. The half-life of phenytoin is less than 20 h in low doses, but is prolonged in high doses, newborn infants and elderly people. The half-life is shortened when phenytoin is given concomitantly with an enzyme-inducing drug, such as phenobarbital or carbamazepine. Phenytoin is effective for treating generalized tonic-clonic seizures, partial seizures with or without generalization, and convulsive status epilepticus. Over the years, many new, and even serious, adverse effects of phenytoin have been recognized. Phenytoin encephalopathy, manifesting as cognitive impairment and a cerebellar syndrome, is an important adverse neurological effect, the development of which depends on the saturation kinetics of phenytoin, individual differences in phenytoin metabolism, an inhibitory effect of certain drugs on phenytoin metabolism, or the ability of certain drugs to displace phenytoin from plasma proteins, leading to an increase in the plasma level of unbound phenytoin. Because of its potentially adverse effects, phenytoin is not recommended as the first choice for treating epileptic seizures, except as a co-drug for managing convulsive status epilepticus. In patients with epilepsy who also have intellectual disability, and are susceptible to balance disturbances and cognitive dysfunction, it is wise to replace phenytoin with another drug, such as carbamazepine or oxcarbazepine. The long-term use of phenytoin is not recommended for patients with loss of locomotion, marked cognitive impairment, or symptoms and signs of cerebellar disease. The prevention of phenytoin intoxication, with the subsequent development of phenytoin-induced encephalopathy, depends on careful observation of the patients and frequent monitoring of plasma levels of phenytoin and other concomitantly administered antiepileptic drugs.

Anticonvulsants↗
PubMed1997

Subcortical type cognitive impairment in herpes zoster encephalitis.

Nine immunocompetent patients with acute herpes zoster encephalitis (HZE) were studied with the help of neurological investigations. All patients were treated with acyclovir. Neuropsychological performance was compared with that of a group of 16 healthy controls. Computed tomography of the head showed infarct-like hypodense lesions in two patients, involving the internal capsule in one case and the temporoparietal cortex and white matter in another. Hypoperfusion shown by single photon emission computed tomography, mostly involving the frontal areas bilaterally, was seen in six of the seven patients examined. Hyperperfusion as seen in herpes simplex encephalitis was not encountered. One patient remained mildly demented, but all the other patients recovered relatively well. Neuropsychological examination after acyclovir treatment showed a decline in memory and speed of cognitive processes, without circumscribed neuropsychological deficits. Six of the nine patients showed behavioural disinhibition, and mood changes were also observed. Memory impairment in HZE was not as global or as severe as is described after encephalitis due to herpes simplex virus. In HZE both the brain perfusion pattern and the neuropsychological test profile showed features compatible with subcortical dysfunction.

Adult↗
PubMed1996

Cognitive decline in patients with symptomatic HIV-1 infection. No decline in asymptomatic infection.

Thirty-six HIV-1-infected predominantly well-functioning subjects were followed up for one year by repeated neuropsychological, clinical neurological, neuroradiological, and immunological examinations. Changes in cognitive performance related to the severity of HIV-1 infection as well as to neuroradiological or immunological changes were studied. A decline in cognitive speed and flexibility was found in symptomatic subjects (ARC, AIDS). The impairment was especially pronounced in patients with progression of brain atrophy. These findings suggest a brain pathology underlying the cognitive decline in ambulatory outpatients with symptomatic HIV-1 infection. A practice effect was found in asymptomatic subjects (ASX, LAS) and in those with unchanged CT/MRI scans. No systematic relationship was found between cognitive change and immunological change.

Adult↗
PubMed1996

Cognitive impairment after acute encephalitis: comparison of herpes simplex and other aetiologies.

OBJECTIVE: To compare the cognitive defects after acute acyclovir treated herpes simplex encephalitis with those after other types of acute encephalitis. METHODS: Seventy seven consecutive patients between 1985 and 1995 and 29 normal controls were studied. Of the 77 patients without concomitant neurological conditions, 17 had herpes simplex, one virus encephalitis (HSVE group), 27 had some other identified aetiology (non-HSVE group), and in 33 patients the cause was unknown. Acyclovir treatment was started less than four days after the first mental symptoms in 12 of 17 patients with HSVE. A thorough neuropsychological assessment was carried out about one month after the onset. RESULTS: The HSVE group had deficits in verbal memory, verbal-semantic functions, and visuoperceptual functions more often than the non-HSVE group. The risk for cognitive defects was twofold to four-fold in the patients with HSVE compared with the non-HSVE patients. Two (12%) of the patients with HSVE and 12 (44%) of the non-HSVE patients were cognitively intact. Six patients with HSVE (46%) and 17 (89%) non-HSVE patients later returned to work. The lesions on CT or MRI were bilateral only in one patient with HSVE. The defects in the three patients with adenovirus infection were severe and resembled the amnesia after HSVE. Cognitive impairment, not previously reported, was found in encephalitis after rotavirus infection and epidemic nephropathy. CONCLUSION: The recovery in the HSVE group was better than expected based on the medical literature. On the other hand there were surprisingly severe cognitive defects in encephalitis after other viruses. With early acyclovir treatment patients with the least severe HSVE were equivalent to those with non-HSV encephalitis with good outcome whereas those with the most severe non-HSV encephalitis were equivalent to those with HSVE with poor outcome.

Acute Disease↗
PubMed1995

Hyperfixation of 99mTc-HMPAO and hypofixation of 123I-iomazenil in acute herpes encephalitis.

We studied two patients with herpes encephalitis (HSE) by [99mTc]HMPAO and [123I]iomazenil single photon emission computed tomography. Increased uptake of HMPAO was seen for up to 63 days in the HSE affected brain area. Iomazenil binds to benzodiazepine receptors and can measure neurone loss. Decreased iomazenil uptake was observed a few days after onset, at a time when hyperfixation of HMPAO occurred. Because in HSE neurone loss occurs simultaneously with hyperfixation of HMPAO, it is unlikely that this hyperfixation is caused by increased neuronal activity, as in epilepsy. This suggests that the hyperfixation of HMPAO in HSE occurs in glia and is sustained by inflammation-related hypermetabolism and acidity. The early neurone loss in HSE stresses the importance of immediate antiviral treatment.

Brain↗
PubMed1995

Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis.

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.

Adult↗
PubMed1993

Tetanus of immunized children.

Five children aged five to 15 years contracted tetanus in Finland between 1969 and 1985, together with 101 adults. Four of the five had been adequately immunized against tetanus. The clinical picture of tetanus was mild or moderate, and none of the children needed respirator treatment. Epilepsy, meningitis and psychogenic symptoms were considered in the differential diagnosis. The course of tetanus in immunized patients is atypical and often benign, but the diagnosis is problematic--in contrast to affected children in developing countries, whose populations are not adequately immunized and where neonatal tetanus is common and often fatal.

Adolescent↗