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Brain dysfunction. Jinghua Jin Department of Neurobiology What you have learned about human brain?. Anatomy? Brain structure? Histology? Cell types? Physiology? Brain function? Pharmacology? Central nervous system drugs ?. Outline.

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brain dysfunction

Brain dysfunction

Jinghua Jin

Department of Neurobiology

what you have learned about human brain
What you have learned about human brain?
  • Anatomy?
    • Brain structure?
  • Histology?
    • Cell types?
  • Physiology?
    • Brain function?
  • Pharmacology?
    • Central nervous system drugs ?
  • I: General conception about human brain
  • II: Cognitive disorder
  • III: Consciousness disorder
  • IV: Summary
1 structural characteristics
1.Structural Characteristics
  • It is located inside the skull, protects brain from injury, confines the brain
  • It is composed of neurons and glial cells
  • The blood supply is from twin vertebral arteries and carotis interna
  • The brain blood barrier protects brain from invasion of toxic insults

Human Brain

To understand the dysfunction of the brain, it’s important to know a bit about the brain…

  • The Brain’s Vital Statistics
  • Adult weight:
    • about 3 pounds (~1.5kg)
  • Adult size:
    • a medium cauliflower
  • Number of neurons:
    • 100 billion
  • Number of synapses:
  • 100 trillion

Specialized Regions of Neurons Carry out Different Functions


Structure of typical mammalian neurons

cellular functions
Cellular Functions
  • Neuron is in charge of different functions
  • Glia nourishes and protects the neurons
how does the synapse carry the signal
How does the Synapse carry the signal?

1. Electrical current travels down the axon

  • Vesicles with chemicals move toward the membrane
  • Chemicals are released and diffuse toward the next cell’s plasma membrane

4. The chemicals open up the transport proteins and allow the signal to pass to the next cell

2 characteristics of metabolism
2. Characteristics of Metabolism
  • The most active organ in energy metabolism
  • Glucose is almost the only source of brain energy
  • The storage of glucose in the brain is very limited
3 characteristics of brain disease
3. Characteristics of Brain Disease
  • Region-dependent consequences to injuries
    • When the cerebral cortex is damaged, the degree of dysfunction is proportionate to the extent of the damage: The more extensive the damage, the more severe the dysfunction is likely to be. However, when the brain stem is damaged, a relatively small amount of damage may cause complete loss of consciousness and even death.
3 characteristics of brain disease1
3. Characteristics of Brain Disease
  • Limited capacity for self repair

Three characteristics of the brain help it compensate and recover after it has been damaged:

    • Redundancy: More than one area can perform the same function.
    • Plasticity: Nerve cells in certain areas can change so that they can perform a different function.
    • Adaptation: Areas with somewhat overlapping functions can sometimes compensate for lost functions.
brain responses to injuries
Brain responses to Injuries
  • Cellular responses:
    • Neuron death (necrosis, apoptosis)
    • Degeneration (axon/dendrites retraction, atrophy )
    • Inflammation (microglia, astrocytes)
    • Demyelination (oligodentrocytes)
  • Functional responses:
    • Acute brain damages will cause disturbance in consciousness: Consciousness disorder
    • Chronic lesions usually lead to cognitive dysfunction: Cognitive disorder
  • I: General conception about human brain
  • II: Cognitive disorder
  • III: Consciousness disorder
  • IV: Summary
1 cognition
  • The ability of the brain to process and store information in order to solve problems.
  • It involves a series of voluntary psychological and social behaviors, such as study, memory, language, thinking, emotion etc.

Structural Basis of Cognition

Cerebral cortex

Brodmann Mapping (52 areas)

function of cerebral cortex
Function of cerebral cortex
  • Frontal cortex: voluntary movements, complex intellectual activities such as writing, memory, creativity, judgment, vision and social responsibility.
    • Lesions in this area will result in contralateral hemiplegia (偏瘫), agraphia (失写症)and frontal dementia (痴呆).
    • Damage in Broca’s area (44 and 45) result in motor aphasia (Broca’s aphasia)
function of cerebral cortex1
Function of cerebral cortex
  • Parietal cortex: plays major role in high level process and integration of sensory information.
    • Lesions in this area produce controlateral sensory deficits.
    • Lesions in the angular gyrus (角回) result in alexia (失读症).
    • Lesions in the supamarginal gyrus (缘上回) result in astereognosis (实体感觉缺失).
function of cerebral cortex2
Function of cerebral cortex
  • Temporal cortex: sensory receiving area for auditory impluses.
    • Lesions in area 22 (auditory association cortex) can lead to Wernicke’s aphasia
    • Lesions in temporal hippocampus can produce spatial or emotional memory impairment
function of cerebral cortex3
Function of cerebral cortex
  • Occipital cortex: vision
    • Lesions in the primary visual cortex result in visual fields defects.
    • Lesions in the visual association cortex result in a lack of recognition of objects and in distinguishing the difference of animals (cat vs. dog).

2. Cognitive Disorder

  • The disturbance of the mental process related to learning and memory, reasoning and judgment, accompanied by aphasia (失语), apraxia (失用), agonasia (失认) or disturbance in executive functioning
major manifestations
Major Manifestations
  • Learning and memory disorders
  • Aphasia
  • Agonosia
  • Apraxia
  • Dementia
case patient h m
Case: Patient H.M.
  • Patient HM suffered from epilepsy to his medial temporal lobe (MTLs). On September 1, 1953, surgeons removed parts of HM's medial temporal lobe on both sides of his brain. HM lost approximately two-thirds of his hippocampal formation, parahippocampal gyrus, and amygdala. His hippocampus appeared entirely nonfunctional because the remaining 2 cm of hippocampal tissue appears atrophic and because the entire entorhinal (which forms the major sensory input to the hippocampus) was destroyed. Some of his anterolateral temporal cortex was completely destroyed.
  • After the surgery he suffered from severe anterograde amnesia: although his short-term memory was intact, he could not commit new events to long-term memory. According to some scientists, HM is impaired in his ability to form new semantic knowledge but researchers argue over the extent of this impairment. He also suffered moderate retrograde amnesia, and could not remember most events in the 3-4 day period before surgery, and some events up to 11 years before, meaning that his amnesia was temporally graded. However, his ability to form long-term procedural memories was still intact; thus he could, as an example, learn new motor skills, despite not being able to remember learning them.

Learning and memory deficits:

Patient HM: MRI

HM’s lesion includes medial temporal lope structures in addition to hippocampus

(amygdala, entorhinal cortex…)

hm s good news and bad news
HM’s good news and bad news

The surgery had a profound effect on declarative memory

Severe anterograde amnesia

Mild retrograde amnesia

Disability to transfer new short-term memory into long-term memory

But there was no effect on:




Many forms of memory were spared (short-term memory, motor, implicit memory, etc).

3 etiology and pathogenesis
3. Etiology and Pathogenesis
  • Chronic brain damage
  • Chronic systemic diseases
  • Mental and psychic disorder
  • Other factors
chronic brain damage
Chronic Brain Damage
  • Imbalance of regulating molecules in the brain
  • Protein aggregation in the brain
  • Chronic cerebral ischemic injury
  • Environmental and metabolic toxins
  • Cerebral trauma
  • Brain aging
1 imbalance of regulating molecules
(1) Imbalance of Regulating Molecules
  • Dopamine
  • Norepinephrine
  • Acetylcholine (Ach)
  • Glutamate
  • Aberrant neuropeptide
  • Lack of neurotrophic factors


Dopamine Pathway


Dopamine Synthesis and Storage

Tyrosine  L-DOPA  DA

2 protein aggregation in the brain
(2) Protein Aggregation in the Brain
  • Gene mutations
  • Abnormal post-translational modification
  • Infection of slow virus in the brain
mutant huntingtin in huntington s disease
Mutant Huntingtin in Huntington’s disease










  • Cleaved to generate N-terminal polyQ fragments
  • Aggregates form in cytoplasm and in nucleus-amyloid-like conformation
  • Controversy over whether aggregates are toxic or protective
  • Gain of toxic function and/or loss of protective function

Alzheimer’s Disease

  • Gradual memory loss
  • Decline in the ability to perform routine tasks
  • Disorientation
  • Difficulty in learning
  • Loss of language skills
  • Impairment of judgment and planning
  • Personality changes

Senile plaques

Neurofibrillary tangles

3 chronic cerebral ischemic injury
(3) Chronic Cerebral Ischemic Injury
  • Energy exhaustion and acidosis
  • Intracellular calcium overload
  • Free radical injury
  • Excitatory toxicity
  • Inflammatory reaction by cytokine
excitatory toxicity
Excitatory toxicity
  • A general pathologic process beginning with the energy and metabolic dysfunction caused by cerebral ischemia and anoxia, which then result in inhibition of Na+-K+-ATPase in plasma membrane, elevation of extracellular K+ and depolarization of neurons. These changes then cause overdosed release of EAA (excitatory amino acids) into the synaptic cleft and overacitvation of EAA receptor, ultimately over excitement and death of neurons.
4 principles for treatment of cognitive disorders
4. Principles for Treatment of Cognitive Disorders
  • General neuroprotective treatments
  • Maintenance of normal neurotransmitter level
  • Surgery
  • I: General conception about human brain
  • II: Cognitive disorder
  • III: Consciousness disorder
  • IV: Summary
1 consciousness
1. Consciousness
  • The sense of awareness of self and the environment.
  • It consists of two aspects:
    • State of arousal and content of consciousness.
2 consciousness disorder
2. Consciousness Disorder
  • Parenchymal mental disorders in which there is impairment of the ability to maintain awareness of self and environment and to respond to environmental stimuli.
structural basis for consciousness disorders
Structural Basis for Consciousness disorders
  • Dysfunction of brain stem reticular formation
  • Dysfunction of thalamus
  • Dysfunction of cerebral cortex

Major Manifestations





3 etiology and pathogenesis1
3. Etiology and Pathogenesis
  • Acute brain injury
    • eg. Diffuse encephalic infection, diffuse brain trauma, subarachnoid hemorrhage, etc.
  • Acute brain intoxication
  • Intracranial extrusion and destructive lesion
acute brain intoxication
Acute Brain Intoxication
  • Endogeneous toxins injury
    • Alteration in neurotransmitter
    • Aberrant energy metabolism
    • Nerve cell membrane injury
  • Exogenous toxins injury
4 principles of prevention and therapy
4. Principles of Prevention and Therapy
  • Urgent management
  • Making a definite diagnosis as soon as possible
  • Monitoring vital signs and consciousness state
  • Brain protections
  • I: General conception about human brain
  • II: Cognitive disorder
  • III: Consciousness disorder
  • IV: Summary
1 glossary
1. Glossary
  • cognition, cognitive disorder, Broca’s aphasia, Wernicke’s aphasia, hemiplegia,agraphia, apraxia, agonasia, alexia, astereognosis, dementia, consciousness disorder, delirium, confusion, drowsiness, coma, excitatory toxicity.
2 questions
2. Questions
  • 1. What is the characteristics of brain disease?
  • 2. What is the pathogenesis of cognitive disorder?
  • 3. What is the pathogenesis of consciousness disorder?