BMB CASE #1 - LEAH FRENCH

The Doctor, Knowledge of Health and Illness 1 Review the basic organisation of the brain in terms of: hemispheres and lobes of the cortex; cerebellum; midbrain; pons; medulla oblongata; and ventricles. 2 Describe how the cerebral blood flow is controlled and the importance of constant blood flow to brain cells. 3 Describe the major vessels of the cerebral circulation and the regions of the cerebral cortex supplied by the 3 main cerebral arteries. 4 Identify the main arteries of the vertebro-basilar circulation. 5 Describe the neural pathways involved in the control of voluntary movements mentioning the key anatomic landmarks related to these pathways. 6 Describe the main somato-sensory pathways, mentioning the key anatomic landmarks related to these pathways. 7 Describe the structure, location and arrangement of fibre tracts and the blood supply of the internal capsule. 8 Identify the regions (primary, unimodal and multimodal association areas) of the cerebral cortex associated with voluntary movements, somatic sensations and language, and briefly describe their functions. 9 Describe the anatomy of the cerebellum including the different functional regions. 10 Describe the role of the cerebellum in controlling limb movements. 11 Define upper and lower motor neurons and describe the clinical features of upper and lower motor neuron lesions. 12 Describe the main clinical features that differentiate occlusion of one of the 3 main cerebral arteries. 13 Describe and differentiate between the clinical features of unilateral spinal cord, brainstem, internal capsular and cortical lesions. 14 Describe the major subtypes of stroke (haemorrhagic, ischaemic, thromboembolic) and their pathological consequences. 15 Identify the major risk factors of cerebrovascular disease. The Doctor, Law, Ethics and Professional Practice 16 Identify the principles of patient safety in health care organizations. 17 Discuss strategies to promote patient safety in the clinic. 18 Identify the professional obligation to disclose medical harm and adverse events to patients, outlined in the Australian National Open Disclosure Standard (2003). 19 Explain the ethical importance of acknowledging wrongdoing which has caused harm to a patient. The Doctor and Patient 20 Demonstrate competence in exploring a patient's experience of sensory disturbance, muscle weakness or paralysis including: the cardinal characteristics of the symptom and its time course relevant associated symptoms the patient's understanding of, and concerns about, what they are experiencing 21 Demonstrate competence in the physical examination of a patient for the assessment of radicular pain, sensory disturbance, muscle weakness, paralysis or clumsiness in the lower limbs: demonstrate appropriate infection control manoeuvres prior to and after examination of a patient [REVISION] describe the anatomy of the major nerves of the lower limb and the muscle groups of the lower limb relevant to clinical examination prepare a patient appropriately for neurological examination in relation to appropriate explanation, confirmation of consent and patient positioning [REVISION] observe the lower limbs for muscle wasting, fasciculation or abnormal movements, comparing the two sides, then discuss the significance of any abnormal findings assess the tone of all muscle groups in the lower limbs, comparing the two sides, then discuss the significance of any abnormal findings test the power of all muscle groups in the lower limbs, comparing the two sides, then discuss the significance of any abnormal findings test the knee jerks, ankle jerks and plantar reflexes, comparing the two sides, then discuss the significance of any abnormal findings test the sensation in the lower limbs through light touch and pin-prick, as well as position sense at the hallux, using appropriate techniques and comparing the two sides, then discuss the significance of any abnormal findings describe the dermatomes of the trunk and lower limb, as well as the sensory territories of the major nerves of the lower limb recognise the common conditions affecting the nerves of the lower limb and discuss the historical and examination features characteristic of each 22 Demonstrate competence in the physical examination of a patient for the assessment of radicular pain, sensory disturbance, muscle weakness, paralysis or clumsiness in the upper limbs: demonstrate appropriate infection control manoeuvres prior to and after examination of a patient [REVISION] describe the anatomy of the major nerves of the upper limb and the muscle groups of the upper limb relevant to clinical examination observe the upper limbs for muscle wasting, fasciculation or abnormal movements, comparing the two sides, then discuss the significance of any abnormal findings assess the tone of all muscle groups in the upper limbs, comparing the two sides, then discuss the significance of any abnormal findings test the power of all muscle groups in the upper limbs, comparing the two sides, then discuss the significance of any abnormal findings test the biceps jerks, triceps jerks and supinator reflexes, comparing the two sides, then discuss the significance of any abnormal findings test the sensation in the upper limbs through light touch and pin-prick, using appropriate techniques and comparing the two sides, then discuss the significance of any abnormal findings describe the dermatomes of the neck and upper limb, as well as the sensory territories of the major nerves of the upper limb recognise the common conditions affecting the nerves of the upper limb and discuss the historical and examination features characteristic of each 23 Demonstrate competence in exploring a patient's experience of dizziness, fits, faints or 'funny turns' including: the cardinal characteristics of the symptom and its time course; relevant associated symptoms, and the patient's understanding of, and concerns about, what they are experiencing. [REVISION] The Doctor and Health in the Community 24 Describe the general principles of rehabilitation of the older patient with stroke.

1. REVIEW THE BASIC ORGANISATION OF THE BRAIN IN TERMS OF: HEMISPHERES AND LOBES OF THE CORTEX; CEREBELLUM; MIDBRAIN; PONS; MEDULLA OBLO NGATA; AND VENTRICLE S. The dirty mess met my sponge Fibres = PAC BASICS Telencephalon Forebrain Diencephalon cerebrum thalamus hypothalamus

midbrain

Mesencephalon midbrain Metencephalon pons and cerebellum Myelencephalon - medulla Medulla

Relay and processing of sensory info Centre for controlling emotion, ANS and hormone production Processing of visual and auditory data (colliculi) Generation of reflexive somatic motor response () Consciousness (reticulospinal)

Hindbrain

Grey matter: Horns of spinal cord Cerebral cortex Basal ganglia Nuclei in SC and brainstem Fissures: Longtitudinal Transverse

Fibre Types: Commissural L to R (eg: CC) Projection brain to SC (eg: CSp) Association in a hemisphere (eg:uncinated fasciculus)

Sulci Central Parietoocipital Lateral

Gyri

BASAL GANGLIA BG is a functional unit Putamen Globus pallidus Caudate Substanstia nigra Subthalamic nucleus Striatum = caudate + putamen Major input place Decision making, action selection and initiation In x-section they look separated (by IC) Corpus striatum = caudate + putamen + globus striatum Lentiform Nucleus = putamen + globus pallidus Separated from other basal ganglia by the internal capsule

CEREBELLUM See LO9 BRAINSTEM MIDBRAIN

PONS

MEDULLA

VENTRICLES

INTERNAL CAPSULE see LO7

2. DESCRIBE HOW THE CEREBRAL BLOOD FLOW IS CONTROLLED AND THE IMPORTANCE OF CONSTANT BLOOD FLOW TO BRAIN CELLS. 4 main mechanisms control cerebral blood flow: 1. pressure autoregulation poorly understood local vascular mechanism. This normally maintains constant blood flow btw 50-150mmHg. In traumatised brain injury this mechanism is comprimised 2. metabolic autoregulation energy metabolites cause local vasodilation 3. chemical factors PCO2 causes local vasodilation. Hyperventilation can lead to a mean reduction in intracranial pressure of about 50% within 2-30 minutes. When PaCO2 < 25 mmHg there is no further reduction in CBF. Therefore there is no advantage in inducing further hypocapnia as this will only shift the oxygen dissociation curve further to the right, making oxygen less available to the tissues. 4. SNS determines MAP which influences cerebral vascular resistance but only minimally (5-10%)
http://www.anaesthesiauk.com/article.aspx?articleid=100754 Importance: brain stores no energy + completely dependent upon blood glucose as substrate (during a fast brain can use ketones) only able to

withstand very short periods of ischaemia

Brain does not tolerate changes in chemical constituents well (ie too much N, too much neurotransmitter rises or drops CBF cause rises or drops in ICP

3. DESCRIBE THE MAJO R VESSELS OF THE CEREBRAL CIRCULATION AND THE REGIONS OF THE CEREBRAL CORTEX SUPPLIED BY THE 3 MAIN CEREBRAL ARTERIES .

ACA

Longitudinal fissure and mainly runs on medial surface of brain

Pericallosal Callosomarginal

Medial precentral gyrus Medial postcentral gyrus medial frontal anterior4/5 of the corpus callosum medial parietal medial orbital Anterior limb of the internal capsule basal ganglia

MCA

Lateral sulcus and onto the lateral surface of brain

lateral striate or lenticulostriate Superior division

inferior division

M1 - from the termination of the ICA to the bi/trifurcation M2 - the segment running in the lateral (Sylvian) fissure M3 - coming out of the lateral fissure, also known as the operator M4 - cortical portions.

lentiform Nu caudate internal capsule Pre and post central gyri Premotor AA supplemental motor AA Brocas area Posterior parietal AA Visual radiation Temporal lobe Posterior parietal AA 1 Auditory Wernickes area Visual cortex

PCA

Around the cerebral peduncle into the transverse fissure on the base of temporal and occipital lobes CN 3 runs between PCA and sup cerebellar A

Lateral geniculate body Occipital cortex lentiform nucleus midbrain pineal medial geniculate bodies thalamus

Venous Drainage superior sagittal, inferior sagittal, straight, transverse, sigmoid, and occipital sinuses, the confluence of sinuses, and the cavernous, sphenoparietal, superior petrosal, inferior petrosal and basilar sinuses drain into internal jugular. Emmissionary veins drain the scalp into the sinus, they are a common route of infection. Bridging veins from brain to sinus, break in subdural. Cavernous sinus drains everything from face.

4. IDENTIFY THE MAIN ARTERIES OF THE VERT EBRO-BASILAR CIRCULATION. Internal Carotid 1. Bifurcation of CC 2. IC into cranium through carotid canal in temporal bone 3. Cavernous sinus 4. Circle of willis Major branches 1. Ophthalmic 2. Posterior communicating 3. Anterior choroidal

Vertebral Artery 1. Branches from subclavian 2. Travels through transverse foramina C1-C6 3. Foramen magnum 4. Up, forward and medial to medulla 5. Joins together in midline to form Basilar Branches: 1. Meningeal supplies bone and dura of posterior cranial fossa 2. Post and ant spinal branches 3. Post inf cerebellar 4. Medullary branches (paramedian branches of VA)

Basilar Artery 1. Ascends in medial groove of pons 2. At top of pons splits into 2 PCA Branches 1. Ant inf cerebrallar A 2. Sup cerebellar A 3. Pontine branches 4. Labyrinthine long artery that travels with CNVIII to internal ear 5. PCA

Cerebellar Circulation

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5. DESCRIBE THE NEUR AL PATHWAYS INVOLVED IN THE CONTROL OF VO LUNTARY MOVEMENTS MENTIONING THE KEY ANATOMIC LANDMARKS RELATED TO THESE PATHWAYS. CSp = CR P limb IC CP basilar pons where theyre scattered amongst transverse pontine fibre CBulbar = same as above except mostly bilaterally innervated and synapse in brain stem Nu medcullary pyramid D L and A CSp

Corticospinal Tract Voluntary motor control of the limbs and trunk is innervated via the corticospinal tract. UMN originate from the Primary motor cortex (50%) Supplementary motor cortex Premotor cortex Primary Somatosensory cortex Parietal lobe Cingulated gyrus They travel through corona radiata, down the posterior limb of the IC, through the middle section of the cerebral peduncle in the midbrain, through the basilar pons where they are scattered among the transverse pontine fibres and nuclei of the pontine grey matter. They come together again to form the medullary pyramid Some decussate and form the contralateral lateral corticospinal tract Some stay ipsilateral and form the anterior corticospinal tract. The anterior corticospinal tract innervates the axial and proximal limb muscles whereas the lateral corticospinal tract innervates the limbs. The lateral corticospinal tract exits at the correct level by synapsing in the ventral horn of the spinal cord with the LMN ( ). The LMN travels out via the ventral root, into the spinal nerve to innervate skeletal muscle. One LMN innervates one motor unit

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Corticobulbar Tract Voluntary motor control of the face and neck UMN originate from the Primary motor cortex (50%) They travel down the genu of the IC, through the middle section of the ccan synapse on the CN nuclei in the midbrain, pons and medulla CN III and IV in the midbrain CN V, VI, VII in the pons CN IX, X, XI, XII in the medulla This tract innervates CN bilaterally except the lower facial nuclei which are innervated only unilaterally (below the eyes) and CNXII which is unilateral as well CN III, IV, VI may be more complex.

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Tectospinal tract Originate from superior colliculus, cross in the posterior tegmental decussation and distribute to cervical levels Superior colliculus receives input from lots of areas but most organised is the visual cortex Mainly influences trunk/facial motor reflexes in relation to visual inputs. Ie turning away from bright light, away from things flying toward your head travels with anterior CSp tract Reticulospinal Tracts Originates in the pontine and medullary reticular Nu. Pontine is uncrossed and medullary project bilaterally. Projects to axial musculature 1. Integrates information from the motor systems to coordinate automatic movements of locomotion and posture. 2. Facilitates and inhibits voluntary movement, influences muscle tone. 3. Mediates autonomic functions 4. Modulates pain impulses 5. Influences blood flow to lateral geniculate travels with anterior CSp tract

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Rubrospinal Tract Project from the red Nu, cross in the anterior tegmental decussation and distribute to all spinal levels (cervical much more though) Red Nu receives input from upper extremity area of the motor cortex, and also (much less though) lower extremity motor cortex Mainly influences limbs - UL flexion travels with lateral CSp tract Vestibulospinal Tract Originate from the medial and lateral Vestibulo Nu in the pons. Medial project bilaterally Lateral project ipsilateral and is a component of the medial longitudinal fasciculus. Mainly influences trunk - antigravity muscles. These work involuntarily when your centre of gravity changes to keep you from toppling over travels with anterior CSp tract

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6. DESCRIBE THE MAIN SOMATO-SENSORY PATHWAYS, ME NTIONING THE KEY ANATOMIC LANDMARKS RELA TED TO THESE PATHWAYS. DCML = 1: skin CB in dorsal ganglion G/C fasciculus ventral horn 2: D up ML to VPL of thalamus 3: p limb IC to somatosensory ALS = 1: skin CB in dorsal ganglion ventral horn 2: D obliquely and travels up ALS VPL of thalamus 3: p limb IC to somatosensory Dorsal Column Medial Lemniscus (DCML) 1 order neuron travels from the sensory area, cell body in the dorsal ganglion enters the dorsal horn to travel vertically in the gracilus/cuneate fasciculus until it reaches the gracilus/cuneate nd Nu in the medulla. Here it synapses with a 2 order neuron. 2 order neuron decussates and travsels up the dorsal column medial lemniscus on the opposite side. Enters the VPL of the thalamus and rd synapses with the 3 order neuron 3 order neuron travels via the posterior limb of the IC to enter the 1 somatosensory cortex in the post central gyrus. This is responsible for Vibration Conscious proprioception Discriminative touch Pressure Two point discrimination Damage to this pathway results in: 1. Loss of vibration sense 2. Loss of position sense 3. Loss of discriminative touch (tactile agnosia) agraphesthesia (writing on skin) astereognesia (object in hand) stereoanaethesia
rd nd st

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Anteriolateral system st 1 order neuron from the area of sensation, cell body in dorsal ganglion, enters the dorsal horn nd and synapses with 2 order neuron. 2 order neuron decussates over several levels, travels up through the anteriolateral system into the medulla, pons and midbrain. They give off branches to the reticular formation (spinoreticular fibres), the midbrain (spinotectal fibres to deep layers of superior colluculus, spinoperiaqueductal fibres), the hypothalamus (spinohypothalamic), accessory olivary Nu, intralaminar Nu. They eventually synapse with rd the 3 order neurons in the VPL of the thalamus. 3 order neurons travel from the VPL of the thalamus up through posterior limb of the IC to the somatosensory cortex in the post central gyrus. This is responsible for Pain Temperature Crude touch Damage to this pathway results in: 1. Loss of pain and temperature 2 levels below lesion on contralateral side
rd nd

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7. DESCRIBE THE STRUCTURE, LOCATION AND ARRANGEMENT OF FIBRE TRACTS AND THE BLOOD SUPPLY OF THE INTERNAL CAPSULE. Sublentiular = auditory radiation Retrolenticular = optic radiation

8. IDENTIFY THE REGIONS (PRIMARY, UNIMOD AL AND MULTIMODAL AS SOCIATION AREAS) OF THE CEREBRAL CORTEX ASSOCIATED WITH VOLU NTARY MOVEMENTS, SOM ATIC SENSATIONS AND LANGU AGE, AND BRIEFLY DESCRIBE THEIR FUNCTIONS. Multimodal Association Areas: A. Parieto-occipitotemporal Association Area Analysis of spatial coordinate of the body - receives visual input + somatosensory input Wernickes area area for language comprehension Angular gyrus - Area for initial processing of visual language Area for naming objects auditory and visual input B. Prefrontal Association Area Receives input from parietooccipitotemporal AA Important for motor planning, elaboration of thoughts, working memory Output to ... Brocas Area word formation C. Limbic Association Area Found in anterior pole of temporal lobe, ventral frontal lobe, cingulated gyrus Responsible for behaviour, emotions, motivation, emotional drive

Voluntary movements 1 Motor cortex > dedicate to controlling hands and muscles of speech Excitation of one motor cortex neuron usually excites a specific muscle cf a specific muscle Premotor Area Generates a pattern of mvmt. More important than supplementary motor area for fine movement sequences. Sends signals to 1 motor cortex or to basal ganglia. Includes: brocas area, voluntary eye mvmt, head rotation, hand mvmts. Supplementary motor area Elicits bilateral motor action. Body-wide movements, fixation movements of the different segments of the body, positional movements of the head and eyes, and so forth, as background for the finer motor control of the arms and hands by the premotor area and primary motor cortex.

Feedback mechanism of cerebellar influence in Motor control

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Cerebellum Responsible for: sequencing of motor activities Monitors and makes corrective adjustments in the motor activities while they are being executed Learns from motor mistakes to make stronger or weaker output corrections Input: Motor plan via corticopontocerebellar pathway Sensory info from periphery via dorsal, ventral, Output: instantaneous subconscious corrective signals are transmitted back into the motor system to or the levels of activation of specific muscles Important for: running, typing, talking. Loss: VANISH DDT = vertigo, ataxia, nystagmus, intention tremor, slurred speech, hypotonia, dysdiadocokinesia, dysmetria, titubation PINARDS = Past-pointing, intention tremor, nystagmus, ataxia, rebound, dysdiad, slurred speech Basal Ganglia Responsible for: help to plan and control complex patterns of muscle mvmt, control relative intensities of separate mvmts, direction of mvmts, sequencing multiple successive and parallel mvmts for achieving complex motor goals.

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Somatic sensation

Language located in dominant hemisphere L side in 95% Wernickes area (aka general interpretive area, tertiary association area, knowing area, Gnostic area) receives input from the somatic, auditory and visual association areas of both hemispheres via corpus callosum. Most important area for higher brain function/intelligence and interpreting the complicated meanings of different patterns of sensory experience When wernickes is destroyed person cannot perform mathematics, read, think through logical problems. Non dominant side damage to same area decreases enjoyment of music, non verbal visual experiences, spatial relations, body language, intonation in voice. Angular Gyrus most inferior portion of posterior parietal lobe immediately behind wernickes area. Vital for reading. A lesion in this area causes the blockage of visual input into wernickes area and the symptoms of dyslexia (word blindness) where the person can see a word and know its a word but not what it means. Brocas area Premotor speech area responsible for formation of words by exciting simultanesouly the laryngeal muscles, respiratory muscles and muscles of the mouth Motor area for controlling hands More developed on dominant hemisphere R handedness The process of speech involves 1. Formation of thoughts, selection of words Wernickes
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2.

Motor control of vocalisation Brocas

R hearing a word and repeating it L reading a word and speaking it

Language Problems Auditory receptive aphasia (word deafness) - destruction of auditory cortex Visual receptive aphasia (word blindness) - destruction of visual cortex Wernickes aphasia - able to hear and understand, can speak with normal grammar, syntax, rate, intonation and stress, but their language content is incorrect. Unable to formulate the thoughts that are to be communicated. Or, if the lesion is less severe, the person may be able to formulate the thoughts but unable to put together appropriate sequences of words. Global aphasia - damage to wernickes + angular gyrus + inferior temporal gyrus totally demented for language Motor/expressive Aphasia damage to Brocas - can decide what they want to say but cannot force muscles to form words. Destruction of 1 motor cortex, basal ganglia, cerebellum all affect speech

9. DESCRIBE THE ANATOMY OF THE CEREBELLU M INCLUDING THE DIFFERENT FUNCTIONAL REG IONS. 3 main f 1. 2. 3.
n

s: Maintenance of posture and balance Maintenance of muscle tone Coordination of voluntary motor activity

3 main parts: Spinocerebellum Receives afferents proprioception Maintains muscle tone provides the circuitry for coordinating mainly mvmts of the distal portions of the limbs, especially the hands and fingers. Neocerebellum/Cerebrocerebellum Projects to motor cortex Helps plan voluntary mvmts receives virtually all its input from the cerebral motor cortex and adjacent premotor and somatosensory cortices of the cerebrum. transmits its output information in the upward direction back to the brain, functioning in a feedback manner with the cerebral cortical sensorimotor system to plan sequential voluntary body and limb movements Vestibulocerebellum included flocculus and nodulus receives input from vestibular Nu Maintenance of balance and eye mvmts via vestibular Nu

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10. DESCRIBE THE ROL E OF THE CEREBELLUM IN CONTROLLING LIMB MOVEMENTS.

3 peduncles

superior cerebellar peduncle (eff>aff) is aka Brachium Conjunctivum Ventral (anterior) spinocerebellar carries proprioceptive info about the LL golgi tendon organ Rostral spinocerebellar carries proprioceptive info (golgi tendon) about the UL Cerebellothalamic (part of the ascending pathway) 1. cerebellum dorsal thalamus 2. Thalamus 1 motor In this way cerebellum performs its comparator fn. It know the msg sent by the motor cortex (it gets a copy of the CSp and Corticobulbar via the corticopontinecerebellar) and it know the actual action of the muscles (via all the efferents) It then sends back a msg using this pathway; the cerebellothalamic, that is able to alter the motor output. The cerebellorubral pathway does pretty much the same thing, just stops at the red nucleus on the way Cerebellorubral (part of the ascending pathway) 1. cerebellum red nucleus in the midbrain. 2. Red Nu ventrolateral Nu in thalamus. 3. Thalamus 1 motor See above Cerebelloreticular (descending pathway) this is the cerebellar efferent that feeds the reticulospinal tract

Middle cerebellar peduncle (Aff) is aka Brachium Pontis Corticopontinecerebellar - brings motor information to the cerebellum from the frontal lobe. Leaves the 1 motor, descends in the internal capsule along with pyramidal tract fibres. Its axons synapse with cells in the pontine nuclei (1st order neuron). 2nd order neurons to the cerebellum via the middle cerebellar peduncle. This tract brings the cerebellum a copy of the information that the corticobulbar and corticospinal tracts are conveying. The connection is contralateral

Inferior cerebellar peduncle (aff=eff) is aka Restiform Body Nucleocerebellar ? Reticulocerebellar afferent that carries exteroceptive information (visual, olfactory, gustatory, auditory, and tactile stimuli). Olivocerebellar ? Arcuateocerebellar - ? Vestibulocerebellar afferent that carries info from the vestibular nucleus in the pons and medulla. This nucleus is fed by the vestibulococclear nerve. Cuneocerebellar carries proprioceptive info about UL muscle spindles. Dorsal (posterior) spinocerebellar carries proprioceptive info about LL spindle fibres. Cerebellovesticular (aka cerebellofugal) these carry impulses to the vestibular Nu. They feed the vestibulospinal tract.

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Role of Cerebellum in Controlling Limb Efferent cells of cerebellum do not project to the LMN or brainstem/spinal cord local circuits; they instead modify patterns of UMNs. n 1 f is to detect motor error and work to reduce this error during the course of the mvmt (feedback) and during subsequent mvmts of this type (feed-forward) Inputs 1. Motor planning input: Afferents from the cerebral cortices pontine Nu cerebrocerebellum 2. Sensory input: Vestibular Nu in medulla project into vesitbulocerebellum + 4xspinocerebellar tract synapse in dorsal Nu of Clarke and project into spinocerebellum. Ipsilateral via inferior cerebellar peduncle; R cerebellum concerned R half of body. Entire cerebellum receives modulation via Inferior olive + locus ceruleus which participate in n the learning and memory f s of the cerebellum. Projections: Most efferents project from cortex to deep Nu then out onto target. 1. exception is the vestibulocerebellum to vestibular Nu in medulla (which then projects to motor cortex). 2. Cerebrocerebellum dentate Nu superior cerebellar peduncle decussate VNC in thalamus 1 motor cortex + premotor AA 3. Spinocerebellum interposed Nu 4. Vestibulocerebellum fastigial Nu Cerebellar dx disrupt the modulation and coordination of ongoing mvmt. Pts have difficultly producing smooth, well coordinated mvmts cerebellar ataxia Alcohol anterior degeneration of the cerebellar cortex difficulty in LL mvmts Vestibulocerebellum lesion difficutly standing upright and maintaining direction of gaze, nystagmus Spinocerebellar lesions difficulty walking b/c of loss of feedback sensory info Dysdiadochokinesia = inability to perform rapid alternating mvmts Dysmetria = over and under reaching Action/intenetion tremors Cerebrocerebellum Impairment in highly skilled sequences of learned mvmt (speech, musical instrument)

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11. DEFINE UPPER AND LOWER MOTOR NEURO NS AND DESCRIBE THE CLINICAL FEATURES OF UPPER AND LOWER MOTOR NEURON LESIONS. Arranged in 2 tracts Lateral group (distal limb, muscles of head) = Rubrospinal + lateral CSp. Contralateral (mostly) Anteriomedial group (trunk) = anterior CSp + tecto, reticulo, vestibulospinal tracts. Bilateral Originate from 1 somatomotor cortex, or unimodal AAs 1 somatosensory cortex, unimodal AA Brainstem Nu Cranial and spinal motor nerves are two sets of LMN. Originate from the anterior horn or the motor Nu of the CNs 2 types for extrafusal muscle fibres for intrafusal muscle fibres Inputs UMNs Interneurons Sensory input from muscles fibres

UMN lesion Initially there is spinal shock which causes hypotonia and areflexia due to sudden in cortical input. 1. Spastic paresis (more common than paralysis) Spasticity = velocity dependent resistance to passive movement (clasp knife). cf rigidity which is not velocity dependent. Due to removal of inhibitory influences on hyperactive stretch reflexes 2. Hyperreflexia 3. Hypertonia 4. Clonus = rhythmic pattern of contractions due to alternating stretching and unloading of muscle spindles 5. Loss of dexterity 6. Appearance of primitive reflexes positive Babinski sign Atrophy uncommon except when long standing CLASH Horse

LMN lesion 1. Flaccid paralysis (loss of mvmt) more commonly than paresis (weakness) 2. muscle tone (since tone is modulated by MN and also influences MN via monosynaptic reflex arc) 3. Fibrillations or fasciculations (aberrant conduction from damaged neuronal ends and denervation hypersensitivity due to expression of large number of Ach receptors) 4. Areflexes 5. Muscle wasting (due to denervation and disuse) Storm Baby Strength Tone Other Reflexes Muscle mass Babinski's sign

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12. DESCRIBE THE MAI N CLINICAL FEATURES THAT DIFFERENTIATE O CCLUSION OF ONE OF T HE 3 MAIN CEREBRAL ARTERIES. ACA: LL>UL paresis and anaesthesia, personality, primitive reflexes (grasp, snout, palmomental), urinary incontinence MCA M1: UL>LL paresis and anaesthesia, w/b aphasia, alexia, agraphia, acalculia, hemineglect, asterognosia, homonymous hemianopia PCA: homonymous hemianopia, memory defect, visual agnosia, contralateral hemiparesis, alexia out agraphia Supplies these areas Medial precentral gyrus Medial postcentral gyrus medial frontal Thus causes these symptoms 1. Contralateral spastic paralysis of lower leg and foot 2. Contralateral sensory loss of lower leg and foot 3. Personality changes 4. Grasp, snout and palmomental reflexes ** 5. Urinary incontinence (no clear relationship as to why)** Anterior 4/5 of the corpus callosum medial parietal medial orbital Anterior limb of the internal capsule basal ganglia

Anterior Cerebral A

The severity of an ACA stroke is most dependent on where the occlusion occurs in relation to the anterior communicating artery Proximal > distal > bilateral anterior cerebral artery occlusion > = better prognosis than A proximal occlusion is normally well tolerated with little to no symptoms. Grasp, snout and palmomental reflexes Examples of primitive reflexes exhibited by a child, but normally inhibited by the frontal cortex in an adult. Grasp - When an object is placed in the infant's hand and strokes their palm, the fingers will close and they will grasp it. Snout - pouting or pursing of the lips that is elicited by light tapping of the closed lips near the midline Palmomental - twitch of the chin muscle elicited by stroking a specific part of the palm. Incontinence in ACA stroke Damage to the anterior portion of the cingulate gyrus, medial superior frontal gyrus, or the midportion of the superolateral frontal gyrus is thought to result in this sphincter dysfunction. Supplies these areas Occipital Medial temporal visual association cortex Cerebral peduncles Splenium of corpus callosum Symptoms Caused 1. Contralateral homonymous hemianopia 2. Defects in forming new memories 3. Visual agnosia (inability to recognise familiar objects) and prosopagnosia (inability to recognise faces) 4. Contralateral hemiparesis (due to cerebral peduncle infarct - rare) If its in the dominant hemisphere (normally the L) 5. Alexia without agraphia**

Posterior Cerebral A

Alexia without agraphia Inability to read but can write. Caused by an infarct to the L PCA (which perfuses the splenium of the corpus callosum and left visual cortex, among other things). The left visual cortex has been damaged, leaving only the right visual cortex able to process visual information, but it is unable to send this information to the language areas (Broca's area, Wernicke's area, etc.) in the left brain because of the damage to the splenium of the corpus callosum. The patient can still write because the pathways connecting the left-sided language areas to the motor areas are intact. Supplies these areas Internal capsule Lateral precentral gyrus Lateral postcentral gyrus Cortical temporal Wernicke's area angular gyrus Symptoms Caused Contralateral spastic hemiparesis involving face + arms > legs Contralateral hemisensory loss involving face + arms > legs Fluent ( Wernickes) aphasia** Alexia (cannot read) Agraphia (cannot write) Acalculia (cannot calculate) Right sided occlusion: left hemineglect** asterognosis (inability to identify an object by touch out visual imput) Contralateral homonymous hemianopia disruption of the optic radiation in the temporal and parietal white matter. Left sided occlusion: nonfluent (Brocas) aphasia** See lacunar infarct below.
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Middle Cerebral A

Cortical frontal and parietal

Broca's area Basal ganglia

Hemineglect Brain areas in the parietal and frontal lobes are associated with the deployment of attention. Hemineglect will only happen if the damage is on the non-dominant side (R) because the non-dominant side of the body is watched by both sides of the brain, whereas the dominant side of the body is only watched by the non-dominant hemisphere. Said again differently: Right-sided spatial neglect is rare because there is redundant processing of the right space by both the left and right cerebral hemispheres, whereas in most left-dominant brains the left space is only processed by the right cerebral hemisphere. Results in dominant side (L) neglect. Is also accompanied by dominant (L) sided visual neglect. Wernickes aphasia Impairment of the comprehension of written and spoken language; can physically speak and even use words just not in an meaningful way. Nonfluent Brocas aphasia Can comprehend text and spoken language but speech is, speech is difficult to initiate, non-fluent, labored, and halting Lacunar Strokes Stroke resulting from occlusion of the lenticulostriate arteries (arise from MCA and PCA) that supply the deep structures of the brain. Depending on which has haemorrhaged will determine the clinical signs seen. These vessels always haemorrhage rather than occlude because they are weak and very susceptible to pressure 37% putamen 14% thalamus 10% caudate 16% pons 10% posterior limb of the internal capsule less commonly occur in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum. 5 classic syndromes 1. Pure motor stroke of the posterior limb of IC body face = UL = LL + dysphagia + transient sensory symptoms 2. Ataxic hemiparesis of the posterior limb of IC, basis pontis and corona radiata cerebellar and motor symptoms like weakness, clumsiness, 3. Dysarthria and clumsy hand of the basis pontis dysarthria (speech motor problem1) and clumsiness 4. Pure sensory stroke of the thalamus persistent and transient numbness, tingling, pain, burning, over one side of body 5. Mixed sensorimotor of the thalamus and posterior limb of IC

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13. DESCRIBE AND DIFFERENTIATE BETWEEN THE CLINICAL FEATURES OF UNILATERAL SPINAL CORD, BRAINSTEM, INTERNAL CAPSULAR AND CORTICAL LESIONS. Clues 1. 2. 3. 4. Clinical Picture Intact cranial nerves Motor deficits are monoplegic, para, hemi, or quad Sensory sx are contralateral to motor Sensory level may be present

Unilateral spinal cord lesion (aka brown sequard syndrome)

Brown sequard syndrome lateral compression of SC (hemisection) ipsi/l LMN signs at level of lesion ipsi/l hemiplegia or monoplegia below lesion & UMN signs ipsi/l loss of vibration and proprioception below lesion contra/l loss of pain and temperature below lesion common causes tumour, radiation, knife wound

Brainstem lesion

Crossed hemiplegia cranial nerve defects 1 side motor sx other side Cerebellar findings Nystagmus LMN cranial nerve findings

Midbrain = CN 3 ptosis, dilated, down and out, vertical gaze palsy Pons = horizontal gaze palsy (INO) + unilateral facial numbness (CN5) + unilateral deafness Medulla-pontine angle - nystagmus Medulla = bulbar palsy unilateral facial numbness

Internal capsular lesion

Cortical lesion

Visual field defect Dystonic postures hyperkinesias Face and extremity weakness F = UL = LL 1. Dysphasia expressive, receptive, global, nominal and reading (frontal and tempotal lobe) 2. Cortical sensory loss steeognosis, graphesthesia, loss of 2 point discrimination. (post central gyrus) 3. Face and extremity weakness possible paraesthesia 4. Conjugate gaze palsy 3 gaze centres, 2 in cortex and 1 brainstem. If the eyes deviate together at all the lesion is cortical, and will deviate to the lesion side 5. seizures

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14. DESCRIBE THE MAJ OR SUBTYPES OF STROK E (HAEMORRHAGIC, ISC HAEMIC, THROMBOEMBOL IC) AND THEIR PATHOLOGIC AL CONSEQUENCES. Stroke =: abrupt onset of focal neurological deficit that is attributed to a focal neurological cause. Rupture of blood vessel Mass effect + toxic effect of blood products Focal cerebral ischemia haemorrhagic

Thrombosis, embolism or vasculitis Hypoxia, ischemia, and infarction cerebral blood flow

Global cerebral ischemia

hypoxic ischaemic encephalopahy

Because brain cells lack glycogen, a in blood flow for > a few seconds results in cerebral ischaemia. When blood flow is restored brain tissue can begin to recover and this is called a transient ischemic attack (=: symptoms resolve in < 24hrs). If cessation of flow lasts > few minutes then cerebral infarction occurs

Ischaemia

Global cerebral ischaemia Cause = hypotention, hypoperfusion, low flow states Result = vulnerable neurons go first and eventually all die persistent vegetative state/brain dead. Borderzones are the most vulnerable regions at the limits of the oerlap of blood supply MORPHO brain swells. Acute = (12-24hrs) red neurons + PMN infiltrate subacute = (24-2/52) cell necrosis + M infiltrate, vascular prolif + reactive gliosis Repair = removal of necrotic tissue, loss of CNS structure, gliosis Focal cerebral ischaemia Cause = 1. Thrombosis - most common site of atherosclerosis = carotid bifurcation, origin of MCA, either end of basilar artery a. Hypercoagulopathy s chance of venous ( in the brain) and arterial thrombosis (before or in brain) 2. Embolism origin of clot is most commonly cardiac mural thrombi and MI, A Fib and valvular disease are predisposing factors. Next most common is carotid thrombi. Other = paradoxical emboli a. Cardioembolic (20%) clot forms on the L atrial, ventricular, valvular wall. RF = A fib, MI, prosthetic valves, RHD, ischaemic cardiomyopahy b. Artery to Artery emboli emboli form on atherosclerotic plaque, break off, occlude RF = male, age, smoking, HTN, DM, hypercholesterolemia, arteristis c. Arterial dissection Pathophysiology = cells die via Rx: a. necrosis because of energy failure cells are starved of glucose mitochondria fail to produce ATP 2+ neurons depolarise intracellular [Ca ] s membrane and mitochondrial dysfunction produce free radicals Fever and hyperglycemia worsen prognosis of dying cells b. apoptosis Result = MORPHO: First 6hrs little observed. By 48hrs tissue is pale, soft, swollen. Day2-10 brain becomes gelatinous and friable and the margin btw good and bad tissue is distinct. Day 10- week 3 tissue liquefies leaving a fluid filled cavity. MICRO: after first 12hrs you see ischaemic neuronal change (red neurons) + vasogenic and Cytotoxic oedema. Endothelial and glial cells swell PMN and M infiltrate/activate
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Treatment: aspirin in 48 hours IV tPA in 3 hours Intra-arterial (catheter) release of tPA up to 6 hours Lowering BP. Only when < 185/110 and thrombolytic therapy is anticipated OR when there is also myocardial ischaemia Stroke unit for rehab physcial, OT, speech T, education, Prognosis: 5-10% develop enough brain herniation to cause brain herniation. Oedema peaks on 2-3 day and is present for 10 days. Cerebellar infarct and resultant oedema is particularly bad b/c of compression of brain stem Rx: water restriction, mannitol, craniotomy Haemorrhagic 1 haemorrhages in the brain parenchyma or subarachinoid space are typically caused from CV disease., cf edidural and subdural haemorrhages are 1 ly from trauma . These other ones can also be caused by trauma 1. Intercerebral Haemorrhage Originates in the putamen (50-60%), thalamus, pons, cerebellar. Those originating in the BG are ganglionic haemorrhages cf cerebral haemorrhages. Acute haemorrhages blood compresses parenchyma cavity eventually occurs with red/brown pigment @ rim central core of clotted blood surrounded by glial changes, oedema RF: a. HTN (50%) - HTN accelerates atherosclerosis in large vessels, hyaline atherosclerosis in small to medium vessels. May be associated with aneurysm development b. Coagulation d/o c. Open heart surgery, neoplasm, amyloid angiopathy, vasculitis, fusiform aneurysms, vascular malformations 2. Subarachinoid Haemorrhage Mostly from rupture of saccular (berri) aneurysm Also can be from vascular malformations, extension of a traumatic haematoma, rupture from HTN, bleeding d/o and tumours. Berri aneurysms are found in 2% of people. There are other types of aneurysms: atherosclerotic (fusiform), mycotic, traumatic and dissecting aneurysm. Much less common. RF for Berris: Genetic, smoking, HTN, Lacunar Strokes: a. Pure motor hemiparesis from an infarct in the pos limb of the IC or basis pontis; the face, arm, and leg are almost always involved b. pure sensory stroke from an infarct in the ventrolateral thalamus c. ataxic hemiparesis from an infarct in the base of the pons d. dysarthria and a clumsy hand or arm due to infarction in the base of the pons or in the genu of the IC e. pure motor hemiparesis with motor (Brocas) aphasia due to thrombotic occlusion of a lenticulostriate branch supplying the genu and ant limb of IC and adjacent white matter of the corona radiata.

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15. IDENTIFY THE MAJ OR RISK FACTORS OF C EREBROVASCULAR DISEASE. NONMODIFIABLE Age Gender Race/ethnicity Family history Genetics Ischaemic MODIFIABLE Arterial HTN TIAs Prior stroke Asymptomatic carotid bruit/stenosis Cardiac disease Aortic arch atheromatosis DM Dyslipidemia and hypercholesterolemia Cigarette smoking Alcohol Increased fibrinogen Elevated homocysteine Low serum folate Elevated anticardiolipin antibodies OCP Obesity Atrial Fibrillation Haemorrhage intracerebral or subarachinoid NONMODIFIABLE MODIFIABLE Trauma Rupture of AV malformation Ischaemic stroke HTN
amyloid angiopathy

Recreational drug use Coagulopathy Tumours AV malformation Saccular aneurysm

16. IDENTIFY THE PRI NCIPLES OF PATIENT S AFETY IN HEALTH CARE ORGANIZATIONS. 1. 2. 3. 4. We all make errors all the time The health-care system is making errors in patient care, and patients are suffering adverse events, much more than previously realized. The same error, even a minor one, can have quite different consequences in different circumstances Errors are not intrinsically bad or morally wrong; BUT health-care people expect perfection of themselves, AND our health-care culture often blames the individual, without looking at the wider picture

17. DISCUSS STRATEGIES TO PROMOTE PATIENT SAFE TY IN THE CLINIC. Clinical Handover Handovers occur at shift changes, when clinicians take breaks, when pts are transferred, and on admission, referral or discharge Breakdown of communication is one of the most important contributing factors to adverse events Solution: The QLD Health Patient Safety and Quality Improvement Service (PSQ) has developed a Clinical Handover Strategy 2010-2013 Coronial Management Coroners Act 2003 allows for coronial recommendations 3Cs Correct Patient, Correct Site and Side, Correct Procedure mandatory standard for all invasive procedures performed in QLD public facilities Was revised in 2009 to create a four-step protocol: 1. Patient Identification Check 2. Obtaining and Checking Informed Consent 3. Marking and Verfication of Site and Side 4. Team Final Check Clinical Incident Management Clinical incidents managed according to the Clinical Incident Management Implementation Standard (CIMIS) Informed Consent Obtaining informed consent ensures patient safety Open Disclosure Is ethically and psychologically important for both patients and staff Open Disclosure Standard approved by Australian Health Ministers Advisory Council and strongly endorsed by QLD Health Process: comprises of two components (1) Clinician Open Disclosure and (2) Formal Open Disclosure Formal Open Disclosure: structured process to ensure communication between patient, senior clinician and the organisation.

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18. IDENTIFY THE PRO FESSIONAL OBLIGATION TO DISCLOSE MEDICAL HARM AND ADVERSE EVE NTS TO PATIENTS, OUTLINED IN THE AUST RALIAN NATIONAL OPEN DISCLOSURE STANDARD (2003). Legally Healthcare professionals have a duty to inform patients of any error which has made their condition worse (Naylor v Preston Area Health Authority [1987] 2 All ER 353), especially in situations where a preventable injury will be made worse without further treatment. Saying sorry to a patient is not legally an admission of guilt and cannot be used to prove liability (in Australia). The 6 steps of Disclosure: 1. Initial Open Disclosure Team Meeting prior to patient/family meeting. 2. Planning between Open Disclosure Consultant and clinician involved or unit director. 3. Meeting between patient/family/carer, Open Disclosure Consultant and clinician involved (or unit director). 4. Debrief between Open Disclosure Consultant and clinician involved (or unit director) post patient/family/carer meeting. 5. Report back to Formal Open Disclosure Team this report summarises any commitments given and how these will be followed up. 6. Patient/family/carer support and follow-up of agreed outcomes. The person making the disclosure should be a) be known to the patient; b) be familiar with the facts of the incident and care of the patient; c) be of sufficient seniority to be credible; d) have received training in open disclosure; e) have good interpersonal skills; f) be able to communicate clearly in everyday language; g) be able and willing to offer reassurance and feedback to the patient and his/her support persons; and h) be willing to maintain a medium to long-term relationship with the patient where possible. 19. EXPLAIN THE ETHICAL IMPORTANCE OF AC KNOWLEDGING WRONGDOI NG WHICH HAS CAUSED HARM TO A PATIENT. Ethically there are seven reasons to disclose an error: 1. To prevent further harm to the patient 2. To facilitate patient trust 3. It is consistent with the moral obligation of the patient physician relationship 4. It is consistent with social trends towards transparency 5. It manifests for patients as people 6. It enables patients to seek restitution where appropriate 7. It enables efforts to improve patient safety 20. DEMONSTRATE COMP ETENCE IN EXPLORING A PATIENT'S EXPERIENCE OF SENSORY DISTUR BANCE, MUSCLE WEAKNESS OR PARALYSI S INCLUDING: THE CARDINAL CHARACTERISTICS OF THE SYMP TOM AND ITS TIME COURSE RELEVANT ASSOCIATED SYMPTOMS THE PATIENT'S UNDERS TANDING OF, AND CONC ERNS ABOUT, WHAT THE Y ARE EXPERIENCING

21. DEMONSTRATE COMP ETENCE IN THE PHYSIC AL EXAMINATION OF A PATIENT FOR THE ASSE SSMENT OF RADICULAR PAIN, SENSORY DISTURBANCE, MUSCLE WEAKNESS, PARALYSIS OR CLUMSINESS IN THE LOWER LIMBS: DEMONSTRATE APPROPRI ATE INFECTION CONTRO L MANOEUVRES PRIOR T O AND AFTER EXAMINATION OF A PATIENT [REVISION] DESCRIBE THE ANATOMY OF THE MAJOR NERVES OF THE LOWER LIMB AN D THE MUSCLE GROUPS OF THE LOWER LIMB RELEVANT TO CLI NICAL EXAMINATION PREPARE A PATIENT AP PROPRIATELY FOR NEUR OLOGICAL EXAMINATION IN RELATION TO APPRO PRIATE EXPLANATION, CONFIRM ATION OF CONSENT AND PATIENT POSITIONING [REVISION] OBSERVE THE LOWER LIMBS FOR MUSCLE WASTI NG, FASCICULATION OR ABNORMAL MOVEMENT S, COMPARING THE TWO SI DES, THEN DISCUSS THE SIGNIFICANCE OF AN Y ABNORMAL FINDINGS ASSESS THE TONE OF ALL MUSCLE GROUPS IN THE LOWER LIMBS, COM PARING THE TWO SIDES , THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDING S TEST THE POWER OF ALL MUSCLE GROUPS IN THE LOWER LIMBS, COMPARING THE TWO SI DES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDING S TEST THE KNEE JERKS, ANKLE JERKS AND PLAN TAR REFLEXES, COMPARING THE TWO SIDES, T HEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS
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TEST THE SENSATION IN THE LOWER LIMBS THROUGH LIGHT TOUCH AN D PIN-PRICK, AS WELL AS PO SITION SENSE AT THE HALLUX, USING APPROPRIATE TE CHNIQUES AND COMPARI NG THE TWO SIDES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDING S DESCRIBE THE DERMATO MES OF THE TRUNK AND LOWER LIMB, AS WELL AS THE SENSORY TERRITORIES O F THE MAJOR NERVES OF THE LOWER LIMB RECOGNISE THE COMMON CONDITIONS AFFECTING THE NERVES OF THE LO WER LIMB AND DISCUSS THE HISTORICAL AND EXAMINATION FEATURES CHAR ACTERISTIC OF EACH

22. DEMONSTR ATE COMPETENCE IN THE PHYSICAL EXAMINATI ON OF A PATIENT FOR THE ASSESSMENT OF RA DICULAR PAIN, SENSORY DISTURBANCE, MUSCLE WEAKNE SS, PARALYSIS OR CLU MSINESS IN THE UPPER LIMBS: DEMONSTRATE APPROPRI ATE INFECTION CONTRO L MANOEUVRES PRIOR T O AND AFTER EXAMINATION OF A PATIENT [REVISION] DESCRIBE THE ANATOMY OF THE MAJOR NERVES OF THE UPPER LIMB AND THE MUSCLE GROUPS OF THE UPPER LIMB RELEVANT TO CLINICAL EXAMINAT ION OBSERVE THE UPPER LIMBS FOR MUSCLE WASTI NG, FASCICULATION OR ABNORMAL MOVEMENTS, COMPARING THE TWO SIDES, THEN DISCU SS THE SIGNIFICANCE OF ANY ABNORMAL FIND INGS ASSESS THE TONE OF ALL MUSCLE GROUPS IN THE UPPER LIMBS, COM PARING THE TWO SIDES , THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDING S TEST THE POWER OF AL L MUSCLE GROUPS IN T HE UPPER LIMB S, COMPARING THE TWO SIDES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDING S TEST THE BICEPS JERKS, TRICEPS JERKS AND SUPINATOR REFLEXES, COMPARING THE TWO SI DES, THEN DISCUSS THE SIGNIFIC ANCE OF ANY ABNORMAL FINDINGS TEST THE SENSATION IN THE UPPER LIMBS THROUGH LIGHT TOUCH AND PIN-PRICK, USING APPROPR IATE TECHNIQUES AND COMPARING THE TWO SIDES, THEN DISCUSS THE SIG NIFICANCE OF ANY ABNORMAL FINDINGS DESCRIBE THE DERMATO MES OF THE NECK AND UPPER LIMB, AS WELL AS THE SENSORY TERRI TORIES OF THE MAJOR NERVES OF THE UPPER LI MB RECOGNISE THE COMMON CONDITIONS AFFECTING THE NERVES OF THE UP PER LIMB AND DISCUSS THE HISTORICAL AND EXAMINATION FEATURES CHAR ACTERISTIC OF EACH

23. DEMONSTRATE COMP ETENCE IN EXPLORING A PATIENT'S EXPERIENCE OF DIZZINESS, FIT S, FAINTS OR 'FUNNY TURNS' INCLUDING: THE CARDINAL CHARACTERISTICS OF THE SYMPTO M AND ITS TIME COURSE; RELEVANT ASSOCIATED SYMPTOMS, AND THE PATIENT'S UN DERSTANDING OF, AND CONCERNS ABOUT, WHAT THEY ARE EXPERIENCING. [REVIS ION]

24. DESCRIBE THE GENERAL PRINCIPLES OF REHABI LITATION OF THE OLDE R PATIENT WITH STROKE. Goals of Rehab: Options for Rehab: Specialist inpatient, outpatient or home-based services How it works: Regular team and family meetings are thus mandatory. Appoint a "key person", one member of the team who liaises with the family; this is also often less intimidating to family members.

Team members: (OPSNNSP) Occupational therapists ADLs Physiotherapists work muscles Speech therapists speech, chewing, swallowing n Nurses bladder and bowel f Neuropsychologist for cognitive deficits like impaired memory and concentration, difficulties in planning and problem solving, personality , assessment of capacity Social workers counselling role with pt and next-of-kin, link professionals in arranging and coordinating community resources. Rehabilitation physician team leader and deals with comorbidities (HTN, diabetes), post-stroke depression, pharmacological Rx of spasticity and pain mgmt.

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