Postnatal Causes of Learning Disability (Intellectual Disability)

Postnatal causes of learning or intellectual disability include head injury, infections, neurodegeneration, and toxicities. A study on the causes of developmental disability found bacterial meningitis, child battering, vehicle-related injuries, and otitis media as the most common causes. However, a developmental disability is a broader term that can include motor developmental disabilities too. The results still give us an idea as this overlap heavily with causes of pure intellectual disability. See Table 1.

Table 1: Most Common Causes of Developmental Disability
Bacterial meningitis	31%
Child battering	15%
Motor-vehicle- related injuries	11%
Otitis media	11%
Postnatal causes of developmental disabilities in children aged 3-10 years -- Atlanta, Georgia, 1991. MMWR Morb Mortal Wkly Rep 1996 Feb 16 45 130134

Head injury

1. Traumatic (accidental) brain injury; one of the most preventable causes of intellectual disabilities.
2. The shaken baby syndrome is the most common cause of non-accidental head injury that affects developing brains. 
3. They classify postnatal hypoxia as a perinatal cause if this occurs immediately following birth. However, if it occurs later, we may classify it as another postnatal cause of intellectual disability. 

Infections

1. Meningitis, especially bacterial meningitis, is one of the most common causes of intellectual disability. 
2. Encephalitis, that might be viral can also cause intellectual disability. At a later age, the international classification of disease categories the sequelae of encephalitis under organic mental conditions as a postencephalitic syndrome. 

Degenerative or demyelinating disorders 

Rett syndrome 

Signs of intellectual (learning) disability appear in girls with Rett syndrome at around 18 months to four years of age. Rett syndrome is a genetic disorder that occurs to due MeCP2 gene mutation; it is prenatal, but the appearance of intellectual disability is postnatal. 

Epilepsy

Children with frequent recurrent epileptic fits, for example, those with infantile spasms may develop intellectual disability because of brain injury. Children who experience more frequent fits and those who have more severe seizures are more likely to develop seizures than others. 

Toxic-Metabolic Disorders

Lead poisoning 

Lead poising could occur in areas where they still use lead in gas and other chemicals. Lead poising is a highly preventable cause of intellectual disabilities. 

Malnutrition

Malnutrition is a relevant cause of intellectual disability in countries with chronic malnutrition, it is a rare cause of intellectual disabilities overall, especially in developed countries. 

Environmental Deprivation

Non-stimulating environments impact intellectual development, for example, long-term institutional care. Severe long-term institutional deprivation could more likely cause intellectual disability than less severe brief institutionalisation. 

References

Postnatal Causes of Developmental Disabilities in Children (CDC)

Intellectual Disability: Causes (asha.org)

POSTNATAL CAUSES OF DEVELOPMENTAL DISABILITY. (jwatch.org)

Psychodynamic Themes in Panic Disorder

• Difficulty tolerating anger.

• Physical or emotional separation from a significant person both in childhood and in adult life 

• Situations of increased work responsibilities may trigger it 

• Perception of parents as controlling, shocking, cynical, and demanding 

• Internal representations of relationships involving sexual or physical abuse 

• A chronic sense of feeling trapped 

• A vicious cycle of anger at parental rejecting behavior followed by anxiety that the fantasy will destroy the tie to parents.

• Failure of signal anxiety function in ego related to self fragmentation and self-other boundary confusion 

Risk factors for Parkinsonism

The following are some risk factors for Parkinson's disease. 

1. Pesticide exposure
2. Head injury
3. Drinking well water
4. Agricultural occupation
5. Use of beta-blockers.

The Gene associated with antisocial behaviour

Criminal behavior, lack of guilt, and irritability are typical features of antisocial personality disorder. Evidence suggests that a low-activity variant of the MAO-A gene predisposes to adult antisocial behavior in men, especially in those who faced early adversity^1–4. Catechol-O-methyltransferase enzyme metabolizes dopamine and other monoamines. Its gene, the COMT-gene, occurs in two forms: a high-activity form and a low-activity form. They associate these variants with differential abilities of the prefrontal cortex, especially working memory. People with low-activity form may have a more efficient prefrontal cortex, likely because of the greater dopamine level in the synaptic space^5,6. We have associated serotonin transporter gene variants with neuroticism and a predisposition to depression. The variants may also influence individual response to SSRIs8. APOE4 gene is a risk factor for Alzheimer’s disease (compared to APOE2 and APOE3).

Neurobiology of Panic Disorder

"There is most evidence for changes in Gamma-aminobutyric acid, with lowered cortical Gamma-aminobutyric acid type levels measured by magnetic resonance spectroscopy, and diminished benzodiazepine-receptor binding in the parietotemporal regions in unmedicated patients with panic disorder (Hasler et al., 2008)."

This happens in panic disorder. Gamma-aminobutyric acid is the major inhibitory neurotransmitter in the brain. Benzodiazepine also binds to Gamma-aminobutyric acid type A receptors and increases its firing rate, thus resulting in hyperpolarisation of the cell because of increased chloride influx. So, specific regions in the brain are hyperexcitable in patients with panic disorder.

Summary of Hasler et al. 

Context

Studies have implicated the benzodiazepine receptor system in the pathophysiologic mechanism of panic disorder  by indirect evidence from pharmacological challenge studies and by direct evidence from single-photon emission computed tomography and positron emission tomography neuroimaging studies

1. The benzodiazepine receptor binding potential was decreased in multiple areas of the frontal, temporal, and parietal cortices and was increased in the hippocampus/ parahippocampal region in subjects with panic disorder vs controls
2. The most significant decrease was in the dorsal anterolateral prefrontal cortex; the most significant increase in the hippocampus/parahippocampal gyrus
3. In subjects with panic disorder, the severity of panic and anxiety symptoms correlated positively with benzodiazepine receptor binding in the dorsal anterolateral prefrontal cortex but negatively with binding in the hippocampus/parahippocampal gyrus
4. These data provide evidence of abnormal benzodiazepine–Gamma-aminobutyric acid type A receptor binding in panic disorder, suggesting that basal and/or compensatory changes in inhibitory neurotransmission play roles in the pathophysiologic mechanism of panic disorder. 

Risk Factors for PTSD (Post-Traumatic Stress Disorder)

Risk Factors for Post-Traumatic Stress Disorder

The following description of risk factors also answers QID:919472837474

The best answer would be d) her intelligence quotient. The patient has developed symptoms of post-traumatic stress disorder, including the most specific “intrusive symptoms.” These have occurred after the life-threatening event she went through. Both the international classification of diseases and the diagnostic and statistical manual require such a precipitating factor for making the diagnosis. It is an event that is life-threatening, or according to the diagnostic and statistical manual, one that threatens body-integrity (e.g. rape). One may either be a bystander or directly threatened by the event. However, this factor interacts with other predisposing or vulnerability factors in an individual to trigger the condition. Genetic factors account for about one-third of the vulnerability, according to a study conducted on twins working in the U.S. military. Other notable predisposing factors include female gender, a history of anxiety or depression, lower levels of intelligence, neurotic traits, a history of trauma, and lower social support. Her gender, her history of depression, of experiencing a similar event, and her personality, may all have predisposed her to develop post-traumatic stress disorder. Low and not an elevated level of intelligence predisposes to post-traumatic stress disorder. Thus, her elevated level of intelligence may not have added to her risk.

FAINTS

•      Female Gender, Family History of Psychiatric Illness
•      Anxiety/mood disorder (history of)
•      Intelligence (low)
•      Neuroticism
•      Trauma, history of
•      Social support (poor)