Week 9 - Cerebral Cortex - finished

Question 1

Are the interconnections in the cerebral cortex myelinated or unmyelinated?

Answer 1

Mostly unmyelinated

Question 2

How thick is the cerebral cortex?

Answer 2

2-4mm thick

Question 3

How large is the cerebral cortex in feet?

Answer 3

2.5 square feet

Question 4

How many neurons are in the cerebral cortex?

Answer 4

25 billion

Question 5

Understanding of the cerebral cortex over time:

Answer 5

Detailed microscopic investigation into brain structure began in the 1800’s Really advanced in the 1900’s when we started using electrodes on animals Progressed to human epilepsy pt’s Observed effects of electrode stimulation in particular region > mapping Correlated microscopic architecture with regional mapping Such mapping techniques were used by Brodmann to delineate discreet functional areas → Brodmann’s areas (52) First noted was that we had primary functional areas that evoked a particular response with stimulation Secondary areas evoked a more complex response & often required greater stimulation The third category of cortex is association cortex More recently we use pet scanning which allows greater visualization Allows for sequencing & recruitment pattern information Particularly good with emotional and cognitive stimulation

Question 6

What are the names of each of the areas?

Answer 6

Question 7

What are the divisons of the cerebral cortex according to evolution?

Answer 7

Allocortex

Neocortex

Question 8

Describe the allocortex

Answer 8

Found in animals

Archicortex: hippocampus (1 cell layer)

Paleocortex: olfactory cortex (2 cell layers)

Question 9

Describe the neocortex

Answer 9

Found only in mammals

Particular well developed in humans

Human traits such as problem solving, abstract thought and advanced language.

Question 10

What are the characteristics of the neocortex?

Answer 10

–Sheets of cell bodies organised into 6 layers

–Contains at least one layer of pyramidal cells

–Outer layer, molecular, or layer 1 doesn’t contain neurons but allows for attachment of the pia

–Three divisions:

• Primary functional
• Secondary functional
• Association

Question 11

What are the 6 layers of the neocortex? (dont have to worry too much about this stuff, Dela doesn’t want to go into it much)

What are the connections/circuitry that are associated with these layers?

Answer 11

The six layers are numbered from the outer layer in & can be visualised individually in stained sections

• Layer 1: molecular layer
• Layer 2: external granular layer
• Layer 3: external pyramidal layer
• Layer 4: internal granular layer
• Layer 5: internal pyramidal layer
• Layer 6: multiform layer
• The circuitry of these layers has been well described
• Corticocortical inputs & outputs pass b/w layers 1, 2 & 3
• Subcortical connections to & from layers 3, 4 & 5
• While these layers are the anatomical units of the cortex, functionally the cortex is divided into columns that run perpendicular to the brains surface. We already know this from the homunculous

Question 12

Information on epilepsy:

Answer 12

Epilepsy is a group of neurological disorders characterised by recurrent episodes of convulsive seizures, sensory disturbances, abnormal behaviour, loss of consciousness or all of the above. In many cases the underlying cause is unknown but some known causes include hypoxia, encephalitis, meningitis, trauma, tumour or abscess. In children it more frequently has a genetic or developmental basis, and in adulthood it is more often associated with cerebral trauma.

Epilepsy is characterised by a seizure created by wide spread, uncontrolled discharge or depolarisation of cortical neurons. Seizures commonly begin at a focal point with depolarisation spreading radially from here. The frequency of attacks may range from many times a day to intervals of several years. In predisposed individuals, seizures may occur during sleep or after physical stimulation, such as by a flickering light or sudden loud sound. Emotional disturbances also may be significant triggers. Some seizures are preceded by an aura, but others have no warning symptoms. Most epileptic attacks are brief. They may be localised or general, with or without clonic movements, and are often followed by drowsiness or confusion.

The usefulness of EEG varies; it can be very useful for localizing a focal point during a seizure but is relatively useless outside of this.

Treatment is typically pharmacological and aimed at preventing this depolarisation by the use of neuronal depressants. Treatment may also be surgical particularly in cases of tumour or abscess.

Question 13

Describe Grand Mal Seisures

Answer 13

–LOC

–Generalised involuntary mm. contraction

–Cessation of respiration

–Teeth clenching, tongue biting

–Loss of bladder / bowel function

–Preceding aura is common

–Usually no recollection

Question 14

Describe Petite Mal Seizures

Answer 14

–Sudden, momentary LOC

–Most common in children & teens

–No voluntary movement

–May have mild Cx myoclonus

–May have hypotonia

–Consciousness is rapidly regained

–Pt. may be unaware

Question 15

Describe focal seizures

Answer 15

–Discreet area of abnormal neuronal activity

–Most commonly motor or sensory cortex adjacent to the central sulcus

–Most commonly affects the hand, face or foot

–May be caused by a small, focal brain lesion

Question 16

Describe dementia:

Answer 16

Dementia is defined as a cognitive decline in the absence of reduced consciousness.

Manifestations include; short term memory losses, accidents & reduced problem solving, confusion, disorientation, stupor and impaired judgment and impulses. These may progress to acopia, dyspraxias and chronic personality disintegration including mood & behavioural changes. Many causes have been identified and all result in cortical degeneration, most notably of the frontal lobes. Dementias caused by drug intoxication, hyperthyroidism, pernicious anaemia, subdural haematoma, hydrocephalus, insulin shock and pancreatic tumours can be reversed by treating the condition. Many other forms of dementia including Alzheimer’s or senile dementia and multi-infarct dementia however are progressive, irreversible and incurable.

Alzheimer’s disease is a progressive mental deterioration characterised by confusion, memory failure, disorientation, restlessness, agnosia, speech disturbances, inability to carry out purposeful movement, and hallucinosis. The patient may become hypomanic, refuse food, and lose sphincter control without focal impairment. The disease sometimes begins in middle life with slight defects in memory and behaviour, but the symptoms worsen dramatically after the age of 70.

Although it occurs with equal frequency in men and women, the familial risk is four times that of the general population. Typical pathological features are plaques in the cortex with particular degeneration in layers containing pyramidal ganglion cells. The cerebral cortex atrophies with widening of the cerebral sulci, especially the frontal and temporal regions.

Diagnostic criteria consist of a failure in at least three cognitive functions, including memory, use of language, visuospatial skills, personality, and calculating skills. The symptoms frequently begin with an inability to incorporate new knowledge despite retention of old information, an inability to recall words, and an inability to orient to one’s surroundings. Only palliative treatment is available and death usually occurs 8 to 12 years after the first symptoms appear.

Question 17

Disorders of thought: Describe one

Answer 17

Schizophrenia

Schizophrenia is a complex psychotic disorder that affects approximately 1% of the population. Schizophrenia is diagnosed on the basis of a pattern of symptoms and symptom duration. The criteria for diagnosis can be typically divided into positive and negative symptoms.

Positive symptoms include:

Delusions

Hallucinations

Disordered thought & speech

Bizarre behaviour

Negative symptoms include:

Apathy

Withdrawal

Confusion

Poverty of speech

Question 18

Mood disorders: Describe one

Answer 18

Anxiety

The defining characteristics of anxiety may be subjective or objective. Subjective characteristics include increased tension, apprehension, increased helplessness and feelings of uncertainty, inadequacy, fear, distress, worry and impending doom. Objective characteristics include increased heart rate, dilated pupils, and restlessness, insomnia, poor eye contact, trembling, quivering voice, self-focus, increased perspiration, and expressed concern regarding life events.

An anxiety attack is an acute, psychobiological reaction manifested by intense anxiety and panic. Symptoms include palpitations, shortness of breath, dizziness, faintness, profuse sweating, pallor of the face and extremities and a vague feeling of imminent doom or death. Attacks usually occur suddenly, last from a few seconds to an hour or longer, and vary in frequency from several times a day to once a month.

Treatment consists of reassurance, separation of the individual from anxiety-producing situations, administration of a sedative or anxiolytics if necessary and appropriate psychotherapy, usually cognitive behaviour therapy, to identify the stresses perceived as threatening.

Generalised anxiety disorder is a disorder in which anxiety is the most prominent feature. It differs from panic attacks in that it is not short lived, discreet episodes but rather a more persistent and consistent state of being. The symptoms range from mild, chronic tenseness, with feelings of timidity, fatigue, apprehension and indecisiveness, to more intense states of restlessness and irritability that may lead to aggressive acts, persistent helplessness or withdrawal. In extreme cases, the overwhelming emotional discomfort is accompanied by physical responses, including tremor, sustained muscle tension, tachycardia, dyspnoea, hypertension, increased respiration and profuse perspiration. Other physical signs include changes in skin colour, nausea, vomiting, diarrhoea, restlessness, immobilisation, insomnia and changes in appetite, all occurring without identification of a known underlying organic cause.