Neurologgical Damage from Child Sexual Abuse

Galaburda, Cyril E.; Mar 16 2020
Type of WorkEssay

The medicine of the 19th century proved that masturbation had a deleterious effect on the child's brain development. “In France”, f.i.,

  • “Dr Christian expressed the opinion in 1881 that masturbating children would certainly lose their brains, their health and their life” (Aron & Kempf, 1978).
  • “In Great Britain the physician W.C. Ellis wrote in 1838: ‘The most spread cause of idiocy is the brain and the nervous system weakening based on the harmful habit of onanism’” (Stengers & van Neck, 1998).

Modern medicine proves the same is caused by sex, not by onanism. The victims “of” childhood sexual “abuse” (CSA) are said to have electro-encephalographic (EEG) abnormalities in their brains like

  • “paroxysmal events, asymmetries, and/or regions of focal slowing” in the left hemisphere (Ito et al., 1993) and
  • “temporal lobe epilepsy” (Teicher, 2000),
  • “left hemisphere alpha hypercoherence (showing the left hemisphere cells to be undifferentiated) and right hemisphere theta hypercoherence” (Ito et al., 1998; Black et al., 2002),
  • “non-verbal learning disabilities” (Navalta et al., 2006) “implying left hemisphere (cortical) underdevelopment” (Ito et al., 1993) or
  • “a reduced corpus callosum area” (Teicher et al., 1997; Teicher et al., 2004; de Bellis, Keshavan et al., 1999; de Bellis, Keshavan, Shifflett, Iyengar, Beers et al., 2002),
  • “abnormal T2 [Transferse] relaxation time in the cerebellar vermis” (Anderson et al., 2002),
  • “larger amygdala volumes” (de Bellis, Keshavan, Shifflett, Iyengar, Dahl et al., 2002) and
  • “significantly larger pituitary glands” (Thomas & de Bellis, 2004) to produce (through corticotripin-releasing hormone) more glucocorticoid hormone needed for stress reactions (de Bellis et al., 2011; de Bellis & Zisk, 2011), also
  • “reductions in grey matter (GM) volume of the frontal cortex” (Andersen et al., 2008) and
  • “(the) decreased hippocampal volume” (Bremner et al., 1997; Stein et al., 1997; Driessen et al., 2000; McEwen & Magarinos, 2001; Vythilingam et al., 2002; Sapolsky, 2000) where
  • neurons are supposed to be killed by excessive glucocorticoid (Sapolsky et al., 1990; Gunnar & Nelson, 1994; McEwen & Magarinos, 2001).

However, later research has disproved some of these findings.

Cohen's d-s [a statistical value showing correlation] showed a CSA and a control groups had almost the same performance/verbal IQ (intelligence quotient) difference,

  • “there were no epileptiform events in any of the records of either group”, and
  • “the CSA group did not exhibit increased connectivity in the right hemisphere in the theta band or in the left hemisphere in the alpha band when compared to the non-CSA group” (Black, 2005).

ANOVA [ANalyse Of VAriance] and multiple regression analysis

  • “did not show a difference for left or right amygdala volume between childhood abuse patients and controls” (Bremner et al., 1997; Andersen et al., 2008).
  • Talking about “left hemisphere underdevelopment” (Ito et al., 1993), “several well-controlled studies have failed to replicate these findings in acutely traumatized children” (Bonne et al., 2001) and
  • “did not find the predicted decrease in hippocampal volume” (de Bellis, Keshavan et al., 1999; de Bellis, 2001; de Bellis et al., 2001; Bonne et al., 2001; Carrion et al., 2001; de Bellis, Keshavan, Shifflett, Iyengar, Beers et al., 2002).

In order to resolve such contradictions it is speculated that

  • “subcortical gray matter structures that include the limbic system” outgrow and
  • “mask any effects of traumatic stress in maltreated children”, or
  • that these effects are “dampened” by alcohol abuse, which the adolescent victims “of” CSA are especially subjected to (de Bellis, 2001).

But why GM [Gray Matter] growing doesn't mask those “reductions in GM volume”? And why the “adolescent onset (of) alcohol abuse” must have any effect on left hemisphere differentiation that continues only for the first three to six years of life (Ito et al., 1998)?

It is said the

  • “left hippocampal volume was significantly reduced, but the right hippocampus was relatively unaffected” (Bremner et al., 1997; Stein et al., 1997) though alcohol must “be neurotoxic to the hippocampus” in the right hemisphere too.

Moreover, in one study

  • “there was no correlation within the childhood abuse patients between left or right hippocampal volume and years of alcohol… abuse”, and
  • “there was no significant correlation between years of alcohol abuse and left or right hippocampal volume in the group as a whole” (Bremner et al., 1997).

I can offer a better explanation:

all existing studies of CSA-related neurological damage have been externally and internally invalid.

If “Andersen et al. (2008) reported that frontal cortex GM volume… of the maltreated subjects” having “current and/or past psychiatric diagnoses” (Hart & Rubia, 2012), it doesn't mean the frontal cortex GM volume is abnormal in the “maltreated” subjects that have never had any psychiatric diagnoses.

  • “Browne & Finkelhor (1986) noted that only a minority of both sexually abused (SA) children seen by clinicians and adults with a history of CSA show serious disturbance or psychopathology”, and there is “a large percentage of asymptomatic persons with a history of CSA” (Rind et al., 1998).

The frontal cortex GM volume abnormalities are not generalisable to the latter.

Also medial prefrontal hyporesponsivity and amygdaloid hyperresponsivity

  • (Bremner, Narayan et al., 1999; Bremner, Staib et al., 1999; Lanius et al., 2002; Shin et al., 1999; Shin et al., 2004; Shin et al., 2001),
  • “smaller intracranial, cerebral cortex, prefrontal cortex, prefrontal cortical white matter, and right temporal lobe volumes,.. decreased areas of the corpus callosum and subregions two, four, five, six, and seven, and larger frontal lobe cerebrospinal fluid volumes(, smaller) total brain volume”
    • (de Bellis, Baum et al., 1999; de Bellis, Keshavan, Shifflett, Iyengar, Beers et al., 2002),
  • “enlarged right, left, and total lateral ventricles” (de Bellis, Baum et al., 1999) with the pituitary gland (Thomas & de Bellis, 2004), and
  • “smaller left hippocampal volume relative to the matched controls”
    • (Bremner et al., 1997; Stein et al., 1997; Bremner, Southwick & Charney, 1999; Driessen et al., 2000; Vythilingam et al., 2002)
  • have been found only in the victims “of” CSA diagnosed with post-traumatic stress disorder (PTSD).

The two thirds of the SA group demonstrating “left hemisphere alpha hypercoherence” have PTSD (Ito et al., 1998).

Nevertheless, we know that 10% to 58% of the clinically referred victims “of” CSA have no PTSD

  • (Dubner & Motta, 1999; Lipschitz et al., 1999; McLeer et al., 1994),

and all those neurologic data are not valid for them. F.i.,

“medial prefrontal cortical dysfunction is seen in adults with PTSD, but not in traumatized adults without PTSD

  • (Bremner, Narayan et al., 1999; Shin et al., 1999; Shin et al., 2004).”

Can they be called traumatized then?

PTSD could develop after that neurological damage because

  • “Gilbertson et al. (2002) found that non-trauma exposed monozygotic twins of subjects with combat-related PTSD had reduced hippocampal volume, which strongly suggests that reduced hippocampal volume may be a risk factor for the development of chronic PTSD, rather than a consequence of trauma exposure and PTSD.”

How to summarize these data?

Some “victims of CSA” don't suffer neurological damage, another victims do (and develop PTSD just then). It is quite possible for neurological damage to develop independently of CSA (Rind et al., 1998), even precede CSA (Davies, 1979).

Often CSA-related neurological damage has been discovered without statistical control for non-sexual abuse. The

  • “smaller measurements of the corpus callosum and a trend for smaller total brain volume… with smaller intracranial volume (and bigger) ventricular volume”

were found in SA children that at least had witnessed domestic violence (de Bellis, Baum et al., 1999).

  • “A 12% smaller left hippocampal volume” was found in “adult survivors of severe childhood physical and/or sexual abuse” (Bremner et al., 1997).
  • “Among patients who had been abused, abnormal EEG findings were observed in…
    • 60% of the sample with a reported history of physical abuse, sexual abuse, or both; and
    • 72% of the sample in which serious physical or sexual abuse had been documented” (Teicher, 2000).

The EEG abnormalities like the forgoing

  • “paroxysmal events, asymmetries, and/or regions of focal slowing” and
  • “substantially better performance than verbal (IQ) scores implying left hemisphere underdevelopment”

were found only in the victims “of verified physical and/or sexual abuse” (Ito et al., 1993).

Of course, the victims “of” CSA that have never been physically abused and have never witnessed domestic violence show neither neuroanatomic, nor EEG abnormalities.

One may reject that statistical controlling for child physical abuse has still revealed

  • “abnormal T2 relaxation time in the cerebellar vermis” (Anderson et al., 2002), “temporal lobe epilepsy” (Teicher, 2000),
  • “left hemisphere underdevelopment” (Ito et al., 1998; Navalta et al., 2006),
  • reduced GM, corpus callosum and hippocampal volume (Andersen et al., 2008; Vythilingam et al., 2002) in the victims of CSA, but anyway they've been subjected to
  • “forced contact sexual abuse… in which the subject was forced against her will” (Navalta et al., 2006), to
  • “forced involuntary contact… accompanied by threats of harm to self or others, or feelings of fear or terror” (Anderson et al., 2001; Andersen et al., 2008),
  • “accompanied by force, coercion, or distress” (Ito et al., 1998), and, generally speaking, for these studies
  • “CSA is defined as coercive or unwanted” (Blanco et al., 2014).

No research of CSA has ever been controlled for psychological abuse — like psychological abuse during so-called secondary victimization when

  • “traumatized children are prone to experience novel stimuli, including rules and other protective interventions, as sources of threat, they easily respond to their teachers and therapists as perpetrators (Streeck-Fischer & der Kolk, 2000).”

Nevertheless, if there is no “caregiver” to “provide them with a sense of mastery” and if CSA is really wanted by children it does not harm their brains anyhow.

Lots of people don't believe that children may want to be sexually “abused” (Navalta et al., 2006) but children are sexual beings indeed.

  • 85% of CSA cases are neither coercive, nor forced (Lanyon, 1986),
  • in more than 64% children participate (Virkkunen, 1981),
  • in more than 40% children are initiators (Mohr et al., 1964; Rossman, 1976; Bernard, 1982; Kilpatrick, 1992).

More than a half (54%) of 12-year-olds who reported sexual contacts with an adult described it as a positive experience (Lahtinen et al., 2014),

  • “but less than half of (15-years-olds reporting such contacts) perceived these experiences as sexual abuse” (Helweg-Larsen & Larsen, 2006).

Sex that is wanted by children is on no account abusive and has no more deleterious effects on their brain development than does onanism. On the contrary, the brain and the skin develop from the same germ layer, and the brain develops only when the skin is stimulated through groping (Norlik, 2013).

Being sexually “abused” in childhood is inevitable yet, because

  • “up to 50% of women have experienced sexual arousal while breastfeeding —
  • and 8% admitted to having orgasms”
    • (Moorhead, 2016; Polomeno, 1999; Downey, 2014; Griffiths, 2016; Silverberg, 2017).

Such “abusive” reactions are not incidental since they make the mother's nipples erect, and

  • “the observed increase in nipple length due to stimulation may lead to more effective sucking and even more stimulation for mother” to produce more milk (Martinson, 1994).

What happens when children are “protected” from sexual “abuse”?

Like in America where a mother was imprisoned for telling her neighbour about being sexually aroused during breastfeeding (Goodyear-Smith, 1993)? Comparisons of rats handled and non-handled by their mothers as pups have

  • “demonstrated significant and tissue-specific differences in (brain) glucocorticoid receptor binding capacity as a function of handling… It seems that the increase in glucocorticoid receptor sites in the hippocampus is a critical feature for the handling effect”(Francis et al., 1996).
  • “Plotsky & Meaney (1993) found that by separating newborn rats from their mothers repeatedly led to an increase in the production of stress hormones which resulted in decreased hippocampal size.”

Also, in humans subjected to CSA

  • “corpus callosum (is) no smaller when controlled for neglect” (Teicher et al., 2004).
  • “If we assume that lots of attention, licking, and grooming are the natural state of affairs and that lower levels of attention are a form of neglect,” (Teicher, 2000)

why don't we consider depriving children of sex as a form of neglect?