The following power point concerns with Neuro Psychiatric disorders, their causes and treatments.

1. NEUROPSYCHIATRIC DISORDERS
Submitted to- Submitted by-
Department of Zoology Bhavya Vashisht
Kurukshetra University M.Sc. Zoology(F)
Kuruksherta Semester IV
Roll No.4

2. Contents
• Introduction
• Causes
• Types
1. Anxiety and attention deficit hyperactivity disorder
2. Borderline Personality Disorder
3. Multiple Sclerosis
4. Guillain–Barre syndrome
5. Parkinson’s Disease
6. Alzheimer’s Disease
7. Progeria
8. Ischemia
• Conclusion

3. Introduction
• Neuropsychiatry is a field of scientific medicine that concerns itself with
the complex relationship between human behavior and brain function,
and endeavors to understand abnormal behavior and behavioral disorders
on the basis of an interaction of neurobiological and psychological–social
factors.
• These disorders studied under this are called Neuropsychiatric Disorders.
These are-
 Related to dopamine transport (as in Anxiety and attention deficit
hyperactivity disorder)
 Due to brain abnormalities, Adverse childhood experiences,( as in BPD)
 Due to damage in Myelin Sheath (as in Multiple Sclerosis and Guillain–
Barre syndrome)
 Oxidation of molecules such as iron and environmental toxins (as in
Parkinson’s disease)
 Abnormalities in Parts of Brain (as in Alzheimer’s disease)
 Point mutation (as in Progeria)

4. Anxiety and attention deficit
hyperactivity disorder
• Most frequently diagnosed of all neuropsychiatric disorders.
• It can continue through adolescence and childhood
• Symptoms include difficulty staying focused and paying attention,
difficulty in controlling behaviour etc
• ADHD patients has less active frontal lobes of brain which control motor
function, reasoning, judgement, memory etc.

5. Symptoms
• Inattention ( 6 or more)
 Often fails to give close attention to details
 Often has trouble holding attention on tasks or play activities.
 Often does not seem to listen when spoken to directly.
 Often does not follow through on instructions and fails to finish
schoolwork, chores, or duties in the workplace
 Often has trouble organizing tasks and activities.
 Often avoids, dislikes, or is reluctant to do tasks that require mental
effort over a long period of time
 Often loses things necessary for tasks and activities
 Is often easily distracted

6. • Hyperactivity and Impulsivity (6 or more)
 Often leaves seat in situations when remaining seated is expected.
 Often runs about or climbs in situations where it is not appropriate
(adolescents or adults may be limited to feeling restless).
 Often unable to play or take part in leisure activities quietly.
 Often talks excessively.
 Often blurts out an answer before a question has been completed.
 Often has trouble waiting his/her turn.
 Often interrupts or intrudes on others

7. Causes
• The dopamine transporter pumps dopamine out of the synapse back
into cytosol. Dopamine reuptake via DAT provides the primary mechanism
through which dopamine is cleared from synapses.
• The rate at which dopamine transporter(DAT) removes dopamine from the
synapse can have a profound effect on the amount of dopamine in the
cell. The amount of dopamine is reduced that cause ADHD

8. Treatment
• Benzodiazepines are the most widely
prescribed drugs for the treatment of anxiety
• They have side effects like sedation, memory
impairment, and dependence.

9. Borderline Personality Disorder (BPD)
According to I.C.D. by WHO:
Emotionally Unstable Personality Disorder: Personality
disorder whose essential features are a pattern of marked
impulsivity and instability of interpersonal relationships,
and self image.
According to D.S.M. by (APA):
Borderline Personality Disorder: Pervasive pattern of
instability in interpersonal relationship, self image and affects,
as well as marked impulsive behavior.

10. BPD Symptoms
• Emotions
• Self-harm and suicidal behavior
• Interpersonal relationships
• Sense of self
• Cognitions

11. BPD Causes
• Brain abnormalities – less active Prefrontal cortex (regulate emotional
arousal), smaller Amygdala (generation of negative emotions), smaller
Hippocampus (memory)
• Adverse childhood experiences
• Family environment

12. Diagnosis
According to DSM (5 should be present)
 Frantic efforts to avoid real or imagined abandonment.
 A pattern of unstable and intense interpersonal relationships
characterized by alternating between extremes of idealization and
devaluation.
 Unstable self-image or sense of self.
 Impulsivity in at least two areas that are potentially self-damaging
 Recurrent suicidal behavior, gestures, or threats, or self-mutilating
behavior.
 Affective instability due to a marked reactivity of mood
 Chronic feelings of emptiness.
 Inappropriate, intense anger or difficulty controlling anger

13. Treatment
• Psychotherapy
– Removing, modifying or retarding existing symptoms.
– Medicating disturbed pattern of behavior.
– Promoting positive personality growth and development.
• Medications
– Haloperidol (reduce anger)
– Flupenthixol (reduce suicidal behaviour)
– Aripiprazole (reduce depression)

14. Multiple Sclerosis
• Multiple sclerosis is an inflammatory disease in which the
insulating covers of nerve cells in the brain and spinal cord are
damaged.
• This damage disrupts the ability of parts of the nervous
system to communicate, resulting in a wide range
of signs and symptoms, including physical, mental and
sometimes psychiatric problems.

15. Symptoms

16. Causes
• Geography
• Genetics
• Infectious agents
• Pathophysiology (lesions)

17. Treatment
• methyl prednisolone (intravenous
corticosteroid)
• glatiramer acetate (first line treatment)
• Natalizumab reduces the relapse rate

18. Guillain–Barre syndrome (GBS)
• Guillain–Barre syndrome (GBS) is a medical
condition in which there is a rapid-onset weakness of
the limbs
• The disease is usually triggered by an infection which
provokes immune-mediated nerve dysfunction
• Guillain–Barré syndrome is rare, at one to two cases
per 100,000 people annually.

19. Symptoms
 Weakness of the legs and arms
 Muscles of the neck may also be affected
 Weakness of the muscles of the face
 Swallowing difficulties
 Weakness of the eye muscles
 Respiratory failure

20. Causes
• Infection by Campylobacter jejuni,Varicella zoster , Mycoplasma
pneumoniae
• The nerve dysfunction in Guillain-Barré syndrome is caused by an immune
attack on the nerve cells of the peripheral nervous system and their
supportive structures

21. Diagnosis
• A characteristic finding in Guillain-Barré
syndrome is an elevated protein level with low
numbers of white blood cells.

22. Parkinson’s Disease
• Neurodegenerative disorder of the central nervous
system.
• It was discovered by the scientist James Parkinson in
1817. His birthday is now celebrated as Parkinson’s
day i.e. 11th April.
• Parkinson's not only affects humans, but other
primates as well.

23. Symptoms
• Motor symptoms
 Tremor
 Bradykinesia (slowness of movement)
 Rigidity
 Postural insability
• Neuropsychiatric symptoms
 Mood alteration
 Cognition
 Behavior alteration
 Sleep alteration

24. Causes
• 4 theories were given
 Oxidation of molecules such as iron in the Substantia Nigra by
free radicals kill the dopaminergic neurons
 Environmental toxins similar to MPTP (a compound related to
the painkiller Demerol), which have been shown to cause
Parkinsonism-like symptoms, kill the neurons.
 A mysteriously increased rate of dopaminergic neuronal
apoptosis in some individuals
 Genetic influence, as the penetrance of PD has been observed
at higher levels within some families

25. Treatment
• Levodopa- Levodopa has been the most widely used
treatment for over 30 years. L-DOPA is converted into
dopamine in the dopaminergic neurons by dopa
decarboxylase. Since motor symptoms are produced by a lack
of dopamine in the substantia nigra, the administration of L-
DOPA temporarily diminishes the motor symptoms.
• DA- Several dopamine agonists that bind to dopaminergic
post-synaptic receptors in the brain have similar effects to
levodopa.

26. Alzheimer’s Disease
• Alzheimer's disease is a progressive degenerative disease of
the brain. It is first described by the German neuropathologist
Alois Alzheimer (1864-1915) in 1905. This disease worsens
with advancing age, although there is no evidence that it is
cause by the aging process.
• The average life expectancy of a person with the disease is
between five and ten years

27. Causes
• When we study the brain of a Alzheimer's victim, we focus on two specific
areas. One is the cortex of the frontal and cerebral lobes. The second is
the hippocampus which is located below the cerebral cortex and
responsible for short term memory.
• If we study samples of these two section, we would find irregularities

28. Stages of Alzheimer’s disease
1. No clear evidence of memory trouble and deterioration in brain functions.
2. Patient shows very mild memory problems with difficulty in remembering names of friends.
He might make a surprising statement such as inquiring about the health of a friend who
everyone knows, died years ago.
3. There is definite evidence of memory loss, which might interfere with job performance.
4. Clinical evidence of memory impairment when the mental status is tested by doctors. A sign
of this stage is when the patient keeps asking the same question which has already been
answered
5. Patient show problems with both recent and past memories, they even forget events that are
important.
6. Understanding of languages diminishes and simple commands aren't understood. Victims
may go back to their first language if they have one. Eventually languages disappear entirely.
7. Victim becomes bedridden and totally dependent for all functions. Death usually occurs at
this stage form aspiration pneumonia, pneumonia caused by breathing in food or other
objects because the victim doesn't remember how to swallow food safely, or from urinary
infections.

29. Progeria
• Progeria is an extremely rare genetic disorder wherein symptoms
resembling aspects of aging are manifested at a very early age.
• The disorder has a very low incidence rate, occurring in an estimated 1 per
8 million live births.
• Those born with progeria typically live to their mid teens to early twenties.

30. Symptoms
• Scleroderma-like skin condition (a hardening and tightening of
the skin on trunk and extremities of the body).
• Limited growth
• full-body alopecia (hair loss)
• Small face with a shallow recessed jaw, and a pinched nose)
• Atherosclerosis
• Kidney failure
• Loss of eyesight
• Cardiovascular problems.
• Prominent scalp veins
• Prominent eyes

31. Cause
• LMNA gene codes for a structural protein called prelamin A. There
is a farnesyl functional group attached to the carboxyl-terminus of
its structure. The farnesyl group allows prelamin A to attach
temporarily to the nuclear rim. Once the protein is attached, the
farnesyl group is removed.
• Failure to remove this farnesyl group permanently affixes the
protein to the nuclear rim. Without its farnesyl group, prelamin A is
referred to as lamin A. Lamin A, along with lamin B and lamin C,
makes up the nuclear lamina, which provides structural support to
the nucleus
• The cause of progeria was discovered to be a point mutation in
position 1824 of the LMNA gene, in which cytosine is replaced with
thymine

32. Treatment
• A type of anticancer drug, the farnesyltransferase inhibitors (FTIs),
has been proposed, but their use has been mostly limited to animal
models
• Another anti-cancer drug, rapamycin caused removal of progerin
from the nuclear membrane
• Pravastatin and zoledronate are effective drugs when it comes to
the blocking of farnesyl group production.
• However, it is important to remember that no treatment is able to
cure progeria.

33. Ischemia
• Condition in which there is insufficient blood flow to the
brain to meet metabolic demand. This leads to poor
oxygen supply and thus to the death of brain tissue.
• Ischemia leads to alterations in brain metabolism,
reduction in metabolic rates, and energy crisis.
• An interruption of blood flow to the brain for more than
10 seconds causes unconsciousness, and an interruption
in flow for more than a few minutes generally results in
irreversible brain damage.

34. Types
• Focal brain ischemia occurs when a blood clot has occluded
a cerebral vessel. Focal brain ischemia reduces blood flow to a
specific brain region, increasing the risk of cell death to that
particular area.
• Global brain ischemia occurs when blood flow to the brain is
halted or drastically reduced. This is commonly caused
by cardiac arrest

35. Symptoms
• Blindness in one eye
• Weakness in one arm or leg or weakness in one entire
side of the body.
• Dizziness
• Vertigo
• Slurred speech
• Loss of coordination
• Multiple cerebral ischemic events may lead to subcortical
ischemic depression, also known as vascular depression.
This condition is most commonly seen in elderly
depressed patients.

36. Causes
• Sickle Cell Anaemia
• Compression of blood vessels
• Blockage of arteries
• Heart Attack
• Congenital heart defects

37. Treatment
• Alteplase (tpa) is an effective medication for
acute ischemic stroke. When given within 3
hours, treatment with tpa significantly
improves the probability of a favourable
outcome

38. Conclusion
There are many types of neuropsychiatric
disorders. Some of them can be treated but
there is no ultimate cure of them. Treatments
can provide relief but they cannot cure it.

39. THANK YOU