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2.
Minerva Endocrinol ; 33(2): 75-84, 2008 Jun.
Article in English | MEDLINE | ID: mdl-18388853

ABSTRACT

Thyroid dysfunctions may be accompanied by numerous neurological and psychiatric disorders. The most known is cognitive impairment and depression in hypothyroid patients, as well as an increased risk of cerebrovascular accidents. A separate, although a rare entity, is Hashimoto's encephalopathy. In hyperthyroidism there is an increased incidence of psychiatric disorders, including apathetic hyperthyroidism and hyperthyroid dementia. Functional imaging of cerebral blood flow and metabolism helped establish both global and/or regional decrease of both cerebral blood flow and metabolism in hypothyroidism, particularly in regions mediating attention, motor speed and visuospatial processing. Hypothyroid dementia may be mediated by neurocircuitry different from that in major depression. Less is known on flow/metabolism changes in hyperthyroidism. Global blood flow may be slightly increased, with regional deficits of blood flow, particular in hyperthyroid dementia. As presented above radionuclide functional imaging showed some metabolic patterns in thyroid dysfunctions, but still many issues remain unresolved. In particular little is known about the underlying pathology of cognitive impairment and depression in hypothyroidism, which may differ from ones in euthyroid patients. Also little is known about the reversibility of changes in cerebral blood flow following thyroid replacement therapy. In hyperthyroid patients functional imaging might contribute to elucidate the background of apathetic hyperthyroidism and potential different background of psychiatric complications.


Subject(s)
Central Nervous System Diseases/etiology , Hyperthyroidism/complications , Hypothyroidism/complications , Mental Disorders/etiology , Positron-Emission Tomography , Tomography, Emission-Computed, Single-Photon , Brain Diseases/etiology , Cognition Disorders/etiology , Dementia/etiology , Depression/etiology , Hashimoto Disease/complications , Humans , Hyperthyroidism/diagnostic imaging , Hyperthyroidism/psychology , Hypothyroidism/diagnostic imaging , Hypothyroidism/psychology , Positron-Emission Tomography/methods , Stroke/etiology , Tomography, Emission-Computed, Single-Photon/methods
4.
Neurol Neurochir Pol ; 35(6): 1133-40, 2001.
Article in Polish | MEDLINE | ID: mdl-11987708

ABSTRACT

Camptocormia is characterized by pronounced forward flexion of the thoracolumbar spine, which increases while walking and disappears in recumbent position. The clinical spectrum of the described disorders with concomitant camptocormia is heterogenous. It was described for the first time in idiopathic Parkinson's disease in 1999. The pathophysiology of this phenomenon remains unclear but seems to be not related to antiparkinsonian treatment. The authors present the case of a 54 years old woman, with idiopathic Parkinson disease diagnosed 5 years ago. The rapid progression of the disease was associated with good response to Levodopa therapy, although the dose had to be increased up to 1400 mg/d (with peripheral decarboxylase and COMT inhibitor). After 5 years she developed painful spasms of paraspinal muscles which resulted in trunk flexion. The clinical picture resembled the described cases of camptocormia. There was no correlation between the appearance of camptocormia and the regime of levodopa administration (time or dosage). Therefore, one can conclude, that presumably camptocormia is not a form of dystonia of the trunk but, the result of till now unclear other factors (dysfunction in other non-dopaminergic nigrostriatal projections?).


Subject(s)
Parkinson Disease/complications , Posture , Spinal Diseases/diagnosis , Spinal Diseases/etiology , Antiparkinson Agents/therapeutic use , Brain/metabolism , Female , Humans , Levodopa/therapeutic use , Middle Aged , Parkinson Disease/drug therapy , Parkinson Disease/metabolism , Spinal Diseases/drug therapy
5.
Nucl Med Rev Cent East Eur ; 4(2): 73-6, 2001.
Article in English | MEDLINE | ID: mdl-14600888

ABSTRACT

BACKGROUND: We present 4 cases, which illustrate the usefulness of neuroimaging studies in atypical forms of Parkinsonism. Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD) are rare neurodegenerative progressive disorders of the central nervous system of unknown cause. The clinical accuracy in this diagnosis is not very high even in centres specialising in movement disorders. Functional imaging can be helpful in diagnosing PSP and CBD. MATERIAL AND METHODS: We present the results of cerebral blood flow (CBF) SPECT scanning in 2 patients with PSP and 2 patients with CBD. This was performed using a triple-head gammacamera and 99m Tc-HMPAO. RESULTS: In PSP patients a diffuse frontal perfusion deficit was seen, eventually with striatal and occipital hypoperfusion. CT/MRI was either normal or showed a diffuse cortical-subcortical atrophy. In CBD patients left fronto-parieto-temporal cortex and a striatal hypoperfusion were shown. CT scanning was normal in one case and showed an asymmetrical temporo-parietal atrophy in second one. CONCLUSIONS: The pattern of diffuse frontal perfusions deficit in PSP and asymmetrical, contralateral to symptoms of CBD, cortico-subcortical hypoperfusion may be helpful in establishing the correct diagnosis.

6.
Nucl Med Rev Cent East Eur ; 4(2): 123-7, 2001.
Article in English | MEDLINE | ID: mdl-14600899

ABSTRACT

Dementia is one of the main non-motor symptoms of Parkinson's disease (PD) and it is diagnosed in about 30% of cases. Its aetiology remains unclear and contributing factors are controversial. Dementia may be more common in old patients with severe motor symptoms and mild cognitive impairment. Clinico-pathological studies show the association between dementia in PD and the age-related group of dementias, such as AD and VaD. A valuable aid in the assessment of dementia in PD is cerebral blood flow (CBF) brain SPECT scanning. It shows three different patterns of rCBF reduction, including frontal lobe hypoperfusion, Alzheimer-like type of hypoperfusion and multiple, vascular defects. The heterogeneity of rCBF reduction may reflect the multifactorial pathophysiology of dementia in PD. It may result from concomitant AD pathology, cerebrovascular disease, destruction of nigro-striato-frontal projection or may be a distinct disease of different aetiology.

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