Friedrich Nietzsche

1915 ◽  
Vol 61 (252) ◽  
pp. 64-91 ◽  
Author(s):  
Hubert J. Norman

Friedrich Wilhelm Nietzsche was born at Röcken, in Saxony, in 1844. His father was a Lutheran clergyman, and his grandfather held a high official position in the Lutheran Church. His grandmother Nietzsche “came of a family of pastors,” and his mother was the “daughter of a parson”. In view of the strongly antagonistic attitude which Nietzsche afterwards adopted towards the Christian scheme of morality, the marked clerical strain in his ancestry is worthy of note. According to his sister Their ancestors, paternal and maternal, were very long-lived. “Of the four pairs of great-grandparents [one] great-grandfather…reached the age of ninety, five great-grandmothers and great-grandfathers died between seventy-five and eighty-six, two only failed to reach old age. The two grandfathers attained their seventieth year, the maternal grandmother died at eighty-two, and grandmother Nietzsche at seventy-seven.” Nietzsche's mother was also long-lived; she was born in 1826, and was married, in 1843, to Pastor Nietzsche, who was then thirty years old. She died in 1897, “after having suffered ill-health for several years”. Pastor Nietzsche is described by his daughter as being an “extraordinarily sensitive man…any sign of discord, either in the parish or in his own family, was so painful to him that he would withdraw to his study, and refuse to eat or drink, or speak with anybody”. This tendency to seek solitude is worthy of note, as it reappeared in a very marked degree in his son, Friedrich. The father was short-sighted—as was Nietzsche—and, in 1848, this resulted in an accident, the consequences of which were disastrous: he tripped over an obstacle which his defective eyesight had prevented him from observing, and he suffered as a result from concussion of the brain. This shock to the nervous system initiated a train of symptoms—chiefly cerebral—which led to his death eleven months later. The fall may have been the cause of the attack; or, as another biographer says, perhaps “only hastened its approach.” The same writer informs us that Pastor Nietzsche “might have hoped for a fine career had he not suffered from headaches and nerves”. Frau Förster-Nietzsche, however, says that her father had not suffered from headaches prior to the accident. In view of Nietzsche's history, one feels inclined to agree with Halévy, more especially as, where any history of nervous or of mental symptoms of a morbid character are concerned, relatives are usually the last to admit them. Mügge says that Pastor Nietzsche “suffered either from concussion or softening of the brain…doubtless this accident hastened his death”. The youngest of the three children born to Nietzsche's parents, a boy, died just after his second birthday “from teething convulsions”. There was apparently nervous instability in the family; and Ireland says that O. Hansson “learned from a family who knew Friedrich Nietzsche from childhood that a disposition to insanity had been inherited for several generations, both on the father's and the mother's side”. This statement is not in accord with the details of family history as given by Frau Förster-Nietzsche; at the same time, it is, perhaps, no injustice to her to surmise that she was desirous of minimising the pathological aspect of the family heredity, and of laying greater stress upon the more favourable characteristics. When Nietzsche's life-history with its morbid mental vicissitudes is considered, however, it would be surprising if the family annals were found to be clear of all traces of nervous instability.

Children ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. 78
Author(s):  
Anne Bryden ◽  
Natalie Majors ◽  
Vinay Puri ◽  
Thomas Moriarty

This study examines an 11-year-old boy with a known history of a large previously asymptomatic arachnoid cyst (AC) presenting with acute onset of right facial droop, hemiplegia, and expressive aphasia. Shortly after arrival to the emergency department, the patient exhibited complete resolution of right-sided hemiplegia but developed headache and had persistent word-finding difficulties. Prior to symptom onset while in class at school, there was an absence of reported jerking movements, headache, photophobia, fever, or trauma. At the time of neurology consultation, the physical exam showed mildly delayed cognitive processing but was otherwise unremarkable. The patient underwent MRI scanning of the brain, which revealed left convexity subdural hematohygroma and perirolandic cortex edema resulting from ruptured left frontoparietal AC. He was evaluated by neurosurgery and managed expectantly. He recovered uneventfully and was discharged two days after presentation remaining asymptomatic on subsequent outpatient visits. The family express concerns regarding increased anxiety and mild memory loss since hospitalization.


PEDIATRICS ◽  
1965 ◽  
Vol 35 (4) ◽  
pp. 589-595
Author(s):  
John Lorber

1. The family histories of 722 infants who were born with spina bifida cystica were studied. 2. The index cases were referred for surgical treatment and were not selected in any way from the genetic point of view. 3. Intensive inquiries were made to obtain a complete family pedigree, including a prospective follow-up of siblings born after the index case. 4. Of 1,256 siblings 85 or 6.8% had gross malformation of the central nervous system: spina bifida cystica in 54, anencephaly in 22, and uncomplicated hydrocephalus in 9. 5. Of 306 children born after the index case 25 (8%) or 1 in 12 were affected. 6. There was a progressive increase in multiple cases in the family with increasing family size. In sibships of five or more, multiple cases occurred in 24.1%. 7. In 118 families cases of gross malformation of the central nervous system were known to have occurred among members of the family other than siblings. Cases occurred in three generations. 8. It is possible that spina bifida cystica might be a recessively inherited condition.


PEDIATRICS ◽  
1988 ◽  
Vol 82 (6) ◽  
pp. 931-934
Author(s):  
HENRY M. FEDER ◽  
EDWIN L. ZALNERAITIS ◽  
LOUIS REIK

Nervous system involvement in Lyme disease was originally described as meningitis, cranial neuritis, and radiculoneuritis,1-3 but Lyme disease can also involve the brain parenchyma. We describe a child whose first manifestation of Lyme disease was an acute, focal meningoencephalitis with signs and symptoms such as fever, headache, slurred speech, hemiparesis, seizure, and CSF pleocytosis. CASE REPORT A 7-year-old boy was hospitalized Aug 27, 1985, because of hemiparesis. Six weeks prior to admission he had vacationed at Old Lyme, CT. There was no history of rash or tick bite. He had been well until eight hours prior to admission when fever and headache developed.


Author(s):  
Jennifer B. Saunders

This chapter provides information about the significant contexts of the Hindu American community’s narrative performances. Reviewing reasons behind why people immigrate, it begins with general theories of immigration and then concentrates on the specific reasons why Indians left India during the period after 1947. The chapter then shifts its focus to the context in the United States as a receiving site for immigrants from India with particular attention to race and religion, two dominant themes in American immigration that have contributed to the Guptas’ experiences and the dynamics of their community-making activities. This leads to a discussion of the significance of religion for migrants in the United States before introducing the more specific religious context of the Guptas’ community. Finally, the chapter expands its lens to their transnational extended family with family trees, a description of their social community, and a specific history of key players in the family.


Author(s):  
Avindra Nath

It has been nearly three decades since the first descriptions of the neurological comploications of HIV infection. During this period of time there has been tremendous progress in defining the clinical syndromes, modes of diagnosis, detailed pathophysiology and modes of treatment. Many of the dreaded complications are now manageable particularly if diagnosed early. However, neurocognitive impairment associated with HIV infection still remains a significant cause of morbidity and much is needed to control; the effects of the virus on the brain and for the eventual eradication of the virus from the brain reservoir.


Author(s):  
Matthew Wilson Smith

How did we come to think of ourselves not as souls and minds but as nerves and brains? The answer this book gives is a history of the neural subject—that is, a history of a subject understood as primarily and essentially a nervous system. The earliest formation of the neural subject lies at least as far back as Thomas Willis’s Pathology of the Brain, published in 1667, but it is above all during the nineteenth century that the discourse of nerves became foundational for myriad and not always compatible institutions and practices. One of the central institutions in the nineteenth-century rise of the neural subject was the theater, which, because of its peculiarly embodied and social nature, was one of the central sites for the staging and the formation of this subject.


1968 ◽  
Vol 171 (1024) ◽  
pp. 335-352 ◽  

I am afraid that I find a title such as 'The logical analysis of cerebral functions’ irresistible. With what can it be contrasted except ‘The illogical analysis of cerebral functions’ ? Logic is a set of rules that allows one to deduce certain conclusions from certain assumptions. It is best carried out while sitting in an armchair or, nowadays, in a swivel chair in front of a computer console. But, of course, everything depends on the assumptions, and given any set of assumptions it is only a matter of time before, in principle, all possible conclusions can be listed exhaustively. Then, one can compare some of the conclusions with actual empirical results, provided one has the necessary connecting assumptions. This is a classical strategy. But given the peculiar past history and present state of our knowledge about cerebral functions, I am afraid that I am driven to embrace a contrasting approach of an ‘illogical analysis of cerebral functions’. Or, perhaps I should say I prefer an analysis of cerebral function that depends on inference rather than deduction. Deduction is an all-or none affair. It either leads to the brilliant break-through or to the scrap heap, or at least to the repair shop for patching or remoulding. In the history of our subject the scrap merchants have grown rich. I prefer a state of affairs where the assumptions stem from the conclusions rather than the conclusions from the assumptions. The problem of the analysis of cerebral function, as I see it, is that an organism both behaves, with all that can be elaborated by that word, and it also possesses a brain. But the two universes of discourse are quite different—there is nothing that we can say in making an assertion about the possession of a cranium that overlaps with descriptions about behaviour, except that without such a possession no behaviour is displayed for long. That is not a remarkable statement nor even one restricted to possession of an intact cranium: it applies equally forcefully to other vital organs. But somehow we have reached the point where we have more than a shrewd suspicion that the two are not independent—and it is by no means immediately obvious that they are not, as evidenced by the Greek hypothesis that the brain was a device merely for cooling the blood. But how do we study the mutual interaction? I suspect that one rather good way is by following the same steps that have already led us, over the centuries, to the firm view that there is some connexion between brain and behaviour. But progress has been painfully slow, and we are impatient.


2021 ◽  
Vol 2 (1) ◽  
pp. 61-64
Author(s):  
Andrian Fajar Kusumadewi

Introduction : Organic mental disorders are diseases we need to put more attentionon because they are related to systemic disorders or disorders of the brain and cancause high mortality. Organic mental disorders often manifest in the form ofpsychiatric symptoms so that they can be treated too late because the physician isnot able to recognize the symptoms which can be fatal. Sequelae can be found inorganic mental disorders and may affect the patient’s quality of life, so a fast andproper management is needed to get a better outcome. Case presentation: A caseof organic hallucinosis in viral encephalitis had been reported in a 18 year-old malewith a history of sudden changes in behaviour. The symptoms appeared after thepatient had problems during OSPEK and was threatened by someone. The patientwas the only child in the family and often spoiled by his parents. Laboratory andimaging studies showed that there was a cerebritis in the CT scan result, a decreasein CD4 count, and an increase in anti-Rubella IgG titers in which the patient wasfinally diagnosed with viral encephalitis. Conclusion: The diagnosis of organicmental disorders can easily be overlooked in daily clinical practice so that patientsdo not receive proper management


PEDIATRICS ◽  
1968 ◽  
Vol 41 (6) ◽  
pp. 1074-1081
Author(s):  
Beryl D. Corner ◽  
J. B. Holton ◽  
R. M. Norman ◽  
P. M. Williams

An attempt to treat a case of histidinemia using a low histidine protein hydrolysate is described. The diet was started at the age of 7 months in a male infant with severe clinical disorder. The diagnosis was made at 24 weeks, which is the youngest recorded case. Good control of histidine metabolism was achieved. There was an initial improvement in growth rate but very little effect on development otherwise. Death from bronchopneumonia occurred in the fourth year. The brain showed cerebral maldevelopment, likely to be of prenatal origin, as well as typical postepileptic encephalopathy. The etiology of this malformation is discussed in relation to histidinemia and the family history of neurologic disorder.


2013 ◽  
Vol 21 (2) ◽  
pp. 113-119
Author(s):  
G. А. Ushakova ◽  
Y. P. Kovalchuk

We provide a commentary on current experimental and theoretical advances and frame our consideration in terms of the possible functions of MT I+II in the nervous system. Metallothioneins (MT) are a family of small cysteine rich proteins, which since their discovery in 1957 have been implicated in a range of roles including toxic metal detoxification, protection against oxidative stress, and as a metallochaperone involved in the homeostasis of both zinc and copper. The most well studied member of the family is the mammalian metallothionein, which consists of two domains: a β-domain with 9 cysteine residues and an α-domain with 11 cysteine residues. Despite over half a century of research, the exact functions of MT in the nervous system are still unknown. Our studies have shown that the distribution of MT-I+II in the brain after prolonged intoxication, inhalation of 0.1% CdCl2 for 1 hour twice a week over 19 weeks, is dependent on the part of the brain. The metallothionein level declines more than 4 times in the hippocampus 3 weeks after continuous intoxication of 0.1% CdCl2. The level of MT-I+II in the cerebral cortex decreased by 1.5 times compared with the control group and did not change significantly in the cerebellum and thalamus/hypothalamus. The results of an experimental model of postoperative pain indicated that injection with MT-II prevents the development of postoperative hyperalgesia in response to mild alteration of physiological activity. Activation of locomotory and exploratory activity, and decrease of anxiety in rats under MT-II treatment at 100 µg/rat manifests itself on the 4th day after surgery. Our experimental data indicate the multipotent function of MT I+II in the rat brain both as a metal detoxifier and as an inhibitor of postoperative pain. 


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