Depression and calcifications of the basal ganglia: About one case of

被引:0
|
作者
GluckVanlaer, N [1 ]
Fallet, A [1 ]
Plas, J [1 ]
Chevalier, JF [1 ]
机构
[1] HOP RICHAUD, SERV PSYCHIAT PR CHEVALIER, F-78000 VERSAILLES, FRANCE
关键词
athymhormia; basal ganglia; calcifications; depressive disorder; limbic loop; loss of psychic self-activation;
D O I
暂无
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Idiopathic basal ganglia calcifications is a heterogeneous entity characterized by the association of bilateral and symmetric calcifications of the basal ganglia and the dentae nuclei in the cerebellum, polymorphous neuropsychiatric symptomatology. It is rare, of unknown etiology and often hereditary. We report the case of a 48 years old man, who presented with melancholic depression which has been steadily worsening for more than a year and which had led to a serious suicide attempt. Clinical observation revealed apragmatism , affective dullness and impoverished spontaneous expression; the theme of incapacity predominated but guilt feelings were absent. Neurologic examination was normal except for extra-pyramidal signs. CT-scan revealed the presence of bilateral and extensive calcifications of caudate nuclei, lenticular nuclei and thalamus, which indicated a diagnosis of idiopathic basal ganglia calcification characterized by depression. Moreover, MRI revealed an hypersignal of the white periventricular substance. Phospho-calcic results and the parathormone dosage were normal. Psychometric tests showed that although intellectual capacity seemed to be intact, it was not utilised in practice. Unresponsive to antidepressants and sismotherapy, the patient is still the same one and a half year later and needs to remain in an institution. Subsequent tests indicate that intellectual deterioration has begun. This case poses the problem of the relationship between depressive syndrome and basal ganglia lesions. We look at studies bearing on this subject and on other clinically similar syndromes (athymhormia, loss of psychic self-activation), in which the interruption or cortico-striato-pallido-thalamo-cortical circuits (particularly the limbic loop), is a physiopathologic mechanism currently invoked.
引用
收藏
页码:127 / 131
页数:5
相关论文
共 50 条
  • [1] RECURRENT PUERPERAL PSYCHOSIS AND BASAL GANGLIA CALCIFICATIONS - ABOUT ONE CASE
    LUAUTE, JP
    SANABRIA, E
    BIDAULT, E
    LUSSET, P
    MEUNIER, P
    ANNALES MEDICO-PSYCHOLOGIQUES, 1991, 149 (03): : 257 - 261
  • [2] BASAL GANGLIA CALCIFICATIONS IN A CASE OF BIOTINIDASE DEFICIENCY
    SCHULZ, PE
    WEINER, SP
    BELMONT, JW
    FISHMAN, MA
    NEUROLOGY, 1988, 38 (08) : 1326 - 1328
  • [3] A case of Kallmann syndrome with bilateral calcifications at the basal ganglia
    Yanagawa, Youichi
    Okada, Yoshiaki
    NEUROLOGICAL SURGERY, 2007, 35 (02): : 171 - 174
  • [4] BASAL GANGLIA CALCIFICATIONS IN POSTOPERATIVE HYPOPARATHYROIDISM - A CASE WITH UNUSUAL CHARACTERISTICS
    JORENS, PG
    APPEL, BJ
    HILTE, FA
    MAHLER, C
    DEDEYN, PP
    ACTA NEUROLOGICA SCANDINAVICA, 1991, 83 (02): : 137 - 140
  • [5] FAMILIAL ENCEPHALOPATHIES WITH CALCIFICATIONS OF THE BASAL GANGLIA
    GOUTIERES, F
    PRESSE MEDICALE, 1993, 22 (39): : 1948 - 1950
  • [6] BASAL GANGLIA CALCIFICATIONS AND ALS SYNDROME
    SCARPITTA, A
    PISCIOTTA, G
    FIERRO, B
    ITALIAN JOURNAL OF NEUROLOGICAL SCIENCES, 1994, 15 (05): : 249 - 251
  • [7] BASAL GANGLIA INFARCTS WITH CALCIFICATIONS IN CHILDREN
    KAYA, T
    OZKAN, R
    BOZOGLU, N
    ADAPINAR, B
    YAKUT, A
    EUROPEAN JOURNAL OF RADIOLOGY, 1995, 20 (01) : 48 - 51
  • [8] IDIOPATHIC CALCIFICATIONS IN BASAL GANGLIA (FAHRS DISEASE)
    CHATILLON, JD
    DEBILLY, A
    DORMONT, D
    GRIMALDI, A
    BARON, JC
    LEVASSEUR, M
    DINH, ST
    PRESSE MEDICALE, 1988, 17 (34): : 1760 - 1760
  • [9] BILATERAL BASAL GANGLIA CALCIFICATIONS - HYPOPARATHYROIDISM AND SEIZURES
    AURIACOMBE, M
    BERGOUIGNAN, FX
    HENRY, P
    SEMAINE DES HOPITAUX, 1988, 64 (40): : 2599 - 2600
  • [10] BASAL GANGLIA CALCIFICATIONS ON CT - RELATION TO HYPOPARATHYROIDISM
    SACHS, C
    SJOBERG, HE
    ERICSON, K
    NEUROLOGY, 1982, 32 (07) : 779 - 782