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Anatomy of the forebrain theme session

Exam breakdown(?): 15 for anat, 15 for physio, 15 for neurology, 20 for psych

No histology from Kruger, but know the coursepack learning topics for everyone, not just
Kruger. She didnt ask anything about parkinsons, epilepsy, nothing about optic nerve
specifically this refers to the optic vision. All clinical conditions, symptoms syndromes,
Cranial nerves are important where does it come from, which foramen does it go through
those with 2, 3 nuclei these are important what happens if only one nucleus is affected,
what happens when the affected nuclei are shared amongst others. Spinal tracts, upper
motor and lower motor neuron. 3 learning topics in week 1 belongs to Kruger embryo,
spina bifida, motor and sensory function (sans bladder function), congenital malformation of
CNS, anatomy of memory dementia.

Station 1

1. Precentral gyrus, - go look at neuro slides

2. More represented = more precision

3. Giant pyramidal cells corticospinal tract

4. Arise from thalamus, primary motor cortex

5. Function for premotor: planning for motion. Primary = execution of motion

Station 2

1. Check slide

2. What is the function: scanning movement both eyes are conjugate/do the same thing
conjugate movement

3. Right frontal eye field a lesion would result in conjugate deviation to the same side as
the lesion

4. Broca motor, expressive speech expressive aphasia understanding but not able to
verbalize. Expressive part cant write as they lack the inability to express, but the
comprehension is intact. They know that they do not make sense. They cannot use sign
language, as it uses expressive part = physically they can, but cannot express. They can
read and comprehend.

5.

6. Receptive aphasia they do not understand, but form proper words, but no structure
random words. They dont know what theyre speaking. They cannot follow instructions.

7. Global aphasia neither speak nor understand.

Station 3

1. Thalamus

2. Greatest degree of sensitivity and functional importance

3. Receive sensory (primary), interpretive part (association). Receive and interpret signals.

4. Lesion of primary somatosensory: contralateral (hemineglect), sensation would be lost =


lose fine touch and proprioception contralaterally. Pain and temperature is bilateral (little
bit). Main loss would be fine touch and proprioception. (anything in cerebellar uni lesion
= ipsilateral outcome)

5. Loss of integration of sensory impulse = The patient lose integration/interpretation, which


is located in superior parietal cannot interpret special relations = cannot identify
something by touch alone. Requires vision and touch to identify, as compared to touch
alone.

Station 4

1. Posterior temporietal/occipital sulcus, preoccipital notch. NB feature : calcarine sulcus, as


primary visual is near it. Rest is visual association.

2. Function: Vision each side receives contralateral visual field.

3. Number 17 is primary visual cortex. 18 and 19 divides the association.

4. Trauma, ischaemia, tumour. Posterior cerebral artery supplies occipital.

5. Balint syndrome: has 3 distinguishing features: simultanagnosia (inability to perceive the


visual field as a whole cannot see more than 1 object), occulomotoraprexia (lack of
fixation), opticataxia (cant visually guide the hand to pick something up). Patient is basically
blind = can physically see, but cannot see anything than a single object, but cant touch it
or grab it due to opticataxia.

6. Lesion of inferior occipital cortex loss of colour vision

Station 5

1. Temporal (some visual association occurs) there are two important components of the
limbic system
2. Hippocampus/hippocampal complex (dentate and parahippocampal), amygdaloid

3. Olfactory, cingulate gyrus etc look at PPT all yellow parts.

4. Kluver-Bucy syndrome: (amygdaloid body and hippocampal formation removal results in)
docility, loss of ability to learn, excessive exploratory behavior, (male) abnormal, bizarre and
increased sexual activity. Only amygdaloid bodies removed: most of the symptoms, except
sexual activity is not so pronounced. Only hippocampal gyri: (lack of emotional reponse,
special memory and )inability to learn. Removal of entire temporal lobe = Excessive
Exploratory behavior temporal vision association = put everything in mouth = trying to
figure out what stuff is by putting it in the mouth.

5. Medial temporal lobe = main epilotepic(?) focus (epilepsy)

Station 6

1. PPT netters

2. 3 anatomical divisions: anterior, posterior, flocculonodular. Functional divisions:


archicerebellum (flocculonodular with vestigial nucleus), paleocerebellum (vermis and
paravermis with emboliform and globus), neocerebellum (cerebellar hemispheres working
in conjunction with dentate nucleus).

3. Deep cerebellar nuclei:

4. Superior cerebellar tract superior cerebellar midbrain, middle pons, inferior medulla

5. ---------

6. ---------

7. Archicerebellum = balance, cortex of floccuolodular node and vestigial nucleus. Input comes
from vestigial nucleus. Output/efferent is towards the vestigial nucleus (its about balance
and equilibrium). Paleocerebellum: vermis together with globus and emboliform nuclei.
Input is the dorsal and ventral spinocerebellar tract, output is contralateral red nucleus,
cross again to rubrospinal tract, result in ipsilateral due to double decussation. It is
responsible for muscle tone and posture. Neocerebellum: cortex of the cerebellar
hemisphere together with dentate. From the contralateral part of pons, cross over to
neocerebellum, cross over to contralateral part of thalamus, up to motor cortex. Double
decussation = ipsilateral.

Station 7

1. Damage to vermis (part of spinocerebellar pathway): cerebellar ataxia: end up impacting


the medial part of motor tract. Thus, lower limb symptom is present. Posture is affected =
swaying motion. Damaging vermis results in loss of co-ordination of lower limb and trunk.

2. Cerebellar nystagmus: Depending what type results in where the problem is. It is in the
horizontal plane. It is more pronounced when the eyes are looking at one side: most
exaggerated when looking at the side of lesion/ipsilateral. This is due to damage to
flocculonodular.

3. Neocerebellar: dysmetria: wrong length(?) tend to have overshoot/undershoot when


trying to aim something.

4. Adiodochokinesia: rapid alternating movement affected: pronation-supination. Rapid


movement is impacted. NB RAPID

5. Asynergy: lack of co-ordination in complex task such as buttoning up, speed and skills
affected

6. Cerebellar/intention tremor: broad coarse movement, perpendicular to the direction. The


movement is towards the end of the movement.

7. Dysarthria: motor speech disorder slowness, slurring of speech as due to physical inability
to talk.