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DPT Semester 2 > Neurophysiology > Flashcards

Neurophysiology Flashcards

1
Q

<p>What is the function of the Frontal Lobe?</p>

A

<ol> <li>Cognitive function</li> <li>Movement control (primary motor cortex)</li> <li>motor programming of speech (Broca's area)</li></ol>

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2
Q

<p>what are some of the functions of the Parietal lobe?</p>

A

<ol> <li>major sensory center</li> <li>somatosensory integration (temperature, taste, touch and movement)</li> <li>Language comprehension (Wenicke's area)</li></ol>

<p></p>

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3
Q

<p>what are the main functions of the temporal lobe?</p>

A

<ol> <li>memory center</li> <li>auditory center</li> <li>taste, sound, sight and touch integration</li></ol>

<p></p>

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4
Q

<p>what is the main function of the occipital lobe?</p>

A

<p>primary visual center</p>

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5
Q

<p>from most lateral to most medial, what body structures are somatopically mapped at the precentral gyrus?</p>

A

<ol> <li>Mouth <ol> <li>swallowing</li> <li>tongue</li> <li>jaw</li> <li>lips</li> </ol> </li> <li>Face</li> <li>HAND</li> <li>arm</li> <li>Trunk</li> <li>Lower extremity</li></ol>

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6
Q

<p>what body structure would you expect to see somatopically mapped in the longitudinal fissure of the precentral gyrus?</p>

A

<p>(betweenL and R sides)</p>

<p>hip, knee, ankle and toes</p>

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7
Q

<p>from most lateral to most medial, describe where body structures are represented somatopically at the postcentral gyrus</p>

A

<p>most laterally to medially</p>

<ol> <li>intra-abdominal</li> <li>phayrnx</li> <li>mouth</li> <li>Face</li> <li>Arm</li> <li>Trunk</li> <li>Leg (at the top)</li></ol>

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8
Q

<p>what arteries make up the anterior circulation of the brain?</p>

A

<ol> <li>Internal carotid arteries</li> <li>Anterior Cerebral arteries</li> <li>Middle Cerebral arteries</li></ol>

<p></p>

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9
Q

<p>What arteries make up the posterior circulation of the brain?</p>

A

<ol> <li>Vertebral arteries</li> <li>Posterior and Anterior Inferior Cerebellar Arteries</li> <li>Basilar artery</li> <li>Pontine arteries</li> <li>superior cerebellar arteries</li> <li>Posterior Cerebral artery</li></ol>

<p></p>

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10
Q

<p>What are the 3 major arteries that supply our cerebrum?</p>

A

<ol> <li>Anterior Cerebral artery</li> <li>Middle Cerebral artery</li> <li>Posterior Cerebral artery</li></ol>

<p></p>

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11
Q

<p>What areas of the brain are perfused by the anterior cerebral artery?</p>

A

<ol> <li>anterior and medial surface of the brain</li> <li>from frontal lobe to anterior parietal lobe</li> <li>subcortical structures <ol> <li>basal ganglia (anterior internal capsule, inferior caudate nucleus),</li> <li>anterior fornix</li> <li>corpus callosum<span></span></li> </ol> </li></ol>

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12
Q

<p>What are the functions of the areas perfused by the anterior cerebral artery?</p>

A

<ol> <li>frontal lobe→ cognitive and motor functions</li> <li>parietal lobe→ sensory center</li> <li>corpus callosum→ two way highway that allows hemispheres to communicate</li></ol>

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13
Q

<p>what are some signs and symptoms of a stroke involving the Anterior Cerebral Artery?</p>

A

<ol> <li>contralateral hemiparesis or hemiplegia</li> <li>contralateral hemisensory loss</li> <li>apraxia</li> <li>problems w/bimanual tasks</li> <li>sig. cognitive deficits</li> <li>lack of spontaneity, motor inaction, slowness and delay</li> <li>difficulty with executive function tasks</li> <li>transcoritical aphasia</li> <li>contralateral grasp reflex</li> <li>Alien Hand syndrome</li> <li>Urinary incontience</li></ol>

<p></p>

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14
Q

<p>what is contralaleral hemiparesis or hemipelgia?</p>

<p>what brain structures are involved?</p>

A

<ol> <li>weakness effecting one side of the body</li> <li>motor cortex (frontal lobe)</li></ol>

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15
Q

<p>what is apraxia? what brain structures are involved with it?</p>

A

<ol> <li>motor agnosia→ knowledge of how to perform a skilled movement is lost</li> <li>supplementary motor area and corpus callosum</li></ol>

<p></p>

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16
Q

<p>An ACA stroke involving the pre-frontal cortex will include what symptoms?</p>

A

<ol> <li>lack of spontaneity</li> <li>motor inaction</li> <li>slowness and delay</li> <li>difficulties with executive function tasks (attention)</li></ol>

<p></p>

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17
Q

<p>what is transcortical aphasia and what brain structures does it involve?</p>

A

<ol> <li>aphasia→ loss of ability to produce or understand speech <ol> <li>this doesn't tend to be as severe as Broac's apahsia (motor) in that they can function a bit better</li> </ol> </li> <li>supplementay motor area (dominant hemisphere)</li></ol>

<p></p>

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18
Q

<p>what area's/structures of the brain are involved in the contralateral grasp reflex (sucking reflex)?</p>

A

<p>No well understood</p>

<p>maybe corpus callosum and frontal lobe?</p>

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19
Q

<p>what is alien hand syndrome and what regions of the brain are involved with it?</p>

A

<ol> <li>involuntary, uncontrollable movement of the upper limb</li> <li>supplemental motor area</li></ol>

<p></p>

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20
Q

<p>List some ACA treatment strategies</p>

A

<ol> <li>structure environment to minimize external distractions</li> <li>closed chain "big muscle" exercises</li> <li>bimanual activities to tackle UE deficits</li> <li>function-based training</li></ol>

<p></p>

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21
Q

<p>what areas of the brain does the middle cerebral artery (MCA) perfuse?</p>

A

<p>two branches</p>

<ol> <li>entire lateral aspect of the cerebral hemisphere (frontal, temporal, and parietal lobes)</li> <li>subcortical structures, <ol> <li>internal capsule (posterior portion)</li> <li>corona radiata</li> <li>globus pallidus (outer part),</li> <li>most of the caudate nucleus,</li> <li>putamen</li> </ol> </li></ol>

<p></p>

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22
Q

<p>what are the signs and symptoms of MCA syndrome?</p>

A

<ol> <li>Contralateral paresis</li> <li>Contralateral sensory loss</li> <li>Motor speech impairment</li> <li>receptive speech impairment</li> <li>global aphasia</li> <li>perceptual deficits</li> <li>apraxia</li> <li>visual deficits</li> <li>loss of conjugate gaze to opposite side</li> <li>pure motor hemiplegia (lacunar stroke)</li></ol>

<p></p>

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23
Q

<p>what brain structures are involved with motor speech impairment from MCA syndrome?</p>

A

<p>Broca's area (dominant hemisphere)</p>

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24
Q

<p>what brain structures are involved with recepive speech impairment with MCA syndrome?</p>

A

<p>Wenicke's area (dominant hemisphere)</p>

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25
Q

<p>What is global aphasia and what brain structures are involved with it?</p>

A

<ol> <li>also called total apashia <ol> <li>cannot speak fluentyly</li> <li>cannot communicae verbally</li> <li>cannot understand language</li> </ol> </li> <li>Broca's and Wernicke's areas involved</li></ol>

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26
Q

<p>what are some examples of perceptual deficits observed with MCA syndrome?</p>

A

<ol> <li>unilateral neglect→ tendency to behave as if one side of the body and/or one side space does not exist.</li> <li>depth perception issues</li> <li>spatial relations issues</li></ol>

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27
Q

<p>what brain structures are involved with perceptual deficits observed with MCA syndrome?</p>

A

<p>parietal sensory association cortex (non-dominant hemisphere)</p>

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28
Q

<p>what brain structures are involved with visual deficits observed with MCA syndrome?</p>

A

<p>optic radiation in internal capsule</p>

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29
Q

<p>what is "loss of conjugate gaze to opposite side" and what brain structures are involved with it?</p>

A

<ol> <li>conjugate gaze is the ability of the eyes to work together/in unison</li> <li>frontal eye fields or decending tracts</li></ol>

<p></p>

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30
Q

<p>what brain structure are involved with pure motor hemiplegia (lucunar stroke)?</p>

A

<p>upper portion of posterior limb of internal capsule</p>

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31
Q

<p>what are the small perforating arteries off of the MCA?</p>

A

<p>lenticulostriate arteries→ supply deep structures within the cerebrum</p>

<p>basal ganglia and internal capsule</p>

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32
Q

<p>what is a major symptom of a lacunar infarct?</p>

A

<p>pure motor hemiparesis</p>

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33
Q

<p>List some treatment strategies when treating an stroke involving the MCA</p>

A

<ol> <li>Incorperate speech strategies into actions</li> <li>UE functional strengthening</li> <li>sensory reintegration is key</li></ol>

<p></p>

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34
Q

<p>what regions of the brain are perfused by the posterior cerebral artery (PCA)?</p>

A

<ol> <li>occipital lobe</li> <li>posteromedial temporal lobes</li> <li>thalamus</li></ol>

<p></p>

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35
Q

<p>what are some signs and symptoms that would be observed following a PCA stroke?</p>

A

<ol> <li>contralateral homonymous hemianopia</li> <li>cortical blindness</li> <li>visual agnosia</li> <li>prosopagnosia</li> <li>dyslexia</li> <li>memory deficit</li> <li>topographic disorientation</li></ol>

<p></p>

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36
Q

<p>what is homonymous hemianopia? what brain structures are involved with this?</p>

A

<ol> <li>loss of visual information from the same visual field in both eyes</li> <li>visual cortex or optic radiation</li></ol>

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37
Q

<p>what is cortical blindness? What structures/regions of the brain are impacted?</p>

A

<ol> <li>person has no awareness of any visual information due to a lesion in the brain</li> <li>bilateral occiptal lobe</li></ol>

<p></p>

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38
Q

<p>what is visual agnosia? What regions/structures of the brain are involved?</p>

A

<ol> <li>inability to visually recognize objects despite having intact vision</li> <li>occipital lobe (dominant side)</li></ol>

<p></p>

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39
Q

<p>what is prosopagnosia? what regions/structures of the brain are involved?</p>

A

<ol> <li>a highly specific type of visual agnosia→ person is unable to visually ID people's faces, despite being able to correctly interpret emotional facial expressions and being able to visually recognize other items in environment</li> <li>visual association cortex</li></ol>

<p></p>

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40
Q

<p>what region of the brain is involved with dyslexiaresulting from PCA syndrome?</p>

A

<p>dominant calcarine lesion</p>

<p>posterior part of corpus callosum</p>

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41
Q

<p>what regions/structures in the brain are responsible for memory deficits observed with PCA syndrome?</p>

A

<p>lesion ofinferomedial potions of temporal lobe (dominant side)</p>

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42
Q

<p>what is topographic disorientation? what brain regions/structures are involved?</p>

A

<ol> <li>inability to orient in the surrounding and find your way around even in a familiar area</li> <li>nondominant visual area</li></ol>

<p></p>

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43
Q

<p>a stroke involving the PCA and affecting the thalamus would have what symptoms?</p>

A

<ol> <li>central post-stroke (thalamic) pain</li> <li>involuntary movements <ol> <li>choreoarthetosis, intention tremor, hemiballismus)</li> </ol> </li></ol>

<p></p>

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44
Q

<p>describe/define each of the symptoms for a stroke involving the PCA and affecting the thalamus</p>

A

<ol> <li>thalamic pain - neurogenic pain, very hard to control</li> <li>choreoathetosis - involuntary movements</li> <li>hemiballismus - big involuntary movements</li></ol>

<p></p>

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45
Q

<p>List some treatment strategies for PCA syndrome</p>

A

<ol> <li>Gradually increase visual challenges as both symptoms improve and/or pt. is able to habituate to symptoms</li> <li>visual deficts can significantly impact balance</li> <li>remember to give pt visual breaks <ol> <li>eyes closed, shut off lights, etc</li> </ol> </li> <li>may require external aids initially to assist in improving visual deficits</li></ol>

<p></p>

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46
Q

<p>a stroke involving the vertebral arteries and basilar artery is called what?</p>

A

<p>vertebrobasialr artery syndrome</p>

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47
Q

<p>what is a standout symptom to a vertebrobasilar artery stroke?</p>

A

<p>locked-in syndrome</p>

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48
Q

<p>what is locked-in syndrome</p>

A

<p>pt is cognitively intact but loses ALL motion other than eyes</p>

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49
Q

<p>what are NCVs used for?</p>

A

<p>help diagnose nerve damage or disease</p>

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50
Q

<p>what are EMGs used for?</p>

A

<p>help determine if there is myopathic involvement in the disease</p>

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51
Q

<p>List some broad disease categories that electrodiagnostic testing can be helpful in diagnosing</p>

A

<ol> <li>Motor neuron disease</li> <li>Radiculopathy</li> <li>Plexopathy</li> <li>Neuromuscular junction disease</li> <li>Muscle diseases</li> <li>Neuropathies</li> <li>Weakness in ICU</li></ol>

<p></p>

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52
Q

<p>how can you further divide the categeory of neuropathy?</p>

A

<p>mononeuropathy</p>

<p>polyneuropathy</p>

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53
Q

<p>what are the 3 classifications for a mononeuropathy?</p>

A

<ol> <li>Neuropraxia</li> <li>Axonotmesis</li> <li>Neurotmesis</li></ol>

<p></p>

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54
Q

<p>what is neuropraxia?</p>

A

<p>pressure, compression or stretch injury</p>

<p>distorts myelin sheath w/o Wallerian degeneration</p>

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55
Q

<p>what is axonotmesis?</p>

A

<p>demyelination that causes axonal damage</p>

<p>axonal regeneration will occur over time along w/sprouting</p>

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56
Q

<p>What is neurotmesis?</p>

A

<p>severe injury to the nerve</p>

<p>axon, schwann cell and endoneurium are completly disrupted (like a complete cut)</p>

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57
Q

<p>what are the outcome measures we look at when interpreting NCVs?</p>

A

<ol> <li>amplitude</li> <li>latency (proximal and distal)</li> <li>conduction velocity</li></ol>

<p></p>

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58
Q

<p>what is amplitude a measure of?</p>

A

<p>the strength of the AP</p>

<p>related to the # of axons in the nerve being tested</p>

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59
Q

<p>what is latency a measure of?</p>

A

<p>the time it takes the AP to travel</p>

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60
Q

<p>what is conduction velocity a measure of?</p>

A

<p>the velocity of the AP</p>

<p>takes the distance traveled by the AP and the latency into account</p>

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61
Q

<p>when performing an NCV would type of injury would most likely result in changes to latency?</p>

A

<p>demyelination in some capacity</p>

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62
Q

<p>what type of damage to a nerve will affect the conduction velocity?</p>

A

<p>both demyelination and axonal damage</p>

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63
Q

<p>T/F: you can only test motor nerves with NCVs?</p>

A

<p>FALSE</p>

<p>can test both sensory and motor nerves but the set up is a bit different</p>

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64
Q

<p>what is the name for an AP generated during motor nerve testing? sensory nerve testing?</p>

A

<ol> <li>motor→ CMAP (compound motor action potential)</li> <li>sensory→ SNAP (sensory nerve action potential)</li></ol>

<p></p>

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65
Q

<p>SNAPs can be either \_\_\_\_\_\_\_\_\_\_\_\_ or \_\_\_\_\_\_\_\_\_\_\_\_\_\_</p>

A

<p>Orthodromic</p>

<p>Antidromic</p>

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66
Q

<p>what does Orthodromic mean?</p>

A

<p>it is traveling in the natural direction of a sensory AP</p>

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67
Q

<p>what does antidromic mean?</p>

A

<p>testing and recording opposite direction of sensory AP</p>

<p>possible b/c the AP generated during testing will be propogated in both directions</p>

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68
Q

<p>If there is suspected proximal damage what tests would we want to do?</p>

A

<ol> <li>F-wave</li> <li>H-reflex</li></ol>

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69
Q

<p>what is an F-wave?</p>

A

<p>retrograde "rebound" motor impulse</p>

<p>AP that travels the full length of the motor axon and back</p>

<p>(measures the latency of the antidromic CMAP)</p>

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70
Q

<p>T/F: the F-wave can be done on both sensory and motor nerve fibers?</p>

A

<p>FALSE</p>

<p>just motor</p>

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71
Q

<p>what types of damage/diseases is F-wave helpful in diagnosing?</p>

A

<ol> <li>proximal damage/demyelination</li> <li>GBS/CDIP</li> <li>Radiculopathies</li> <li>Peripheral neuropathies</li></ol>

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72
Q

<p>What is an H-reflex?</p>

A

<p>stimualtes an AP that follows the muscle stretch reflex arc</p>

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73
Q

<p>what types of disorders would an H-reflex be helpful in diagnosing?</p>

A

<ol> <li>evaluation of: <ul> <li>nerve root lesions</li> <li>Upper motor neuron lesions</li> </ul> </li> <li>commonly done on the S1 root</li></ol>

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74
Q

<p>what types of diseases/disorders would an EMG test be most helpful in?</p>

A

<p>diseases that affect:</p>

<ol> <li>the muscle (muscular dystrophies)</li> <li>the neuromuscular junction (myasthenia gravis)</li> <li>diffuse disorders that cause peripheal neuropathies</li> <li>disorders that affect the motor neurons in the spinal cord (ALS, ruptured spinal disc)</li></ol>

<p></p>

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75
Q

<p>what does EMG asses?</p>

A

<p>the electrical activity (AP) of the muscle in several stages.</p>

<p>refer to the electical activity as a MUAP (motor unit action potential)</p>

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76
Q

<p>EMG will asses the electrical activity of a muscle in several stages, what are they?</p>

A

<ol> <li>as the needle goes into the muscle (insertional activity)</li> <li>muscle at rest</li> <li>muscle with activation</li></ol>

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77
Q

<p>what type of activity will be observed in a normal/healthy muscle during the at rest phase of an EMG?</p>

A

<ol> <li>insertional activity (50-200 ms =very short)</li> <li>should be silent following the crisp static sound of insertional activity</li> <li>normal spontaneous acitivity may be observed</li></ol>

<p></p>

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78
Q

<p>list some normal spontaneously activity types that can be observed during the EMG at rest</p>

A

<ol> <li>MEPPs - mini end plate potential</li> <li>EPPs - end plate potentials</li> <li>EPSs - end plate spikes</li></ol>

<p></p>

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79
Q

<p>what would be considered abdnormal muscle activity at rest during EMG (3)?</p>

A

<ol> <li>decrease in normal insertional activity</li> <li>increase in normal insertional activity</li> <li>prolonged insertional activity</li></ol>

<p></p>

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80
Q

<p>what can cause a decrease in insertional activity during EMG?</p>

A

<ol> <li>loss of muscle fibers (fibrosis, muslce atrophy)</li> <li>some metabolic disordes</li></ol>

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81
Q

<p>what can cause an increase in insertional activity during EMG?</p>

A

<ol> <li>neuropathic disorders</li> <li>myopathic disorders</li></ol>

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82
Q

<p>what can cause prolonged insertional activity during EMG?</p>

A

<ol> <li>post acute denervation</li> <li>inflammatory muscle disorders</li> <li>muscular dystrophy</li></ol>

<p></p>

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83
Q

<p>what types of abnormal activity can be observed during rest in EMG testing?</p>

A

<ol> <li>Fibrillations</li> <li>Positive Sharp waves</li> <li>Fasciculations</li> <li>Complex regional discharge (CRD)</li> <li>Myokymic</li> <li>Myotonic</li></ol>

<p></p>

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84
Q

<p>what is a fibrillation?</p>

A

<p>spontaneous discharge of one or a few muscle fibers</p>

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85
Q

<p>what are fibrillations associted with?</p>

A

<ol> <li>muscle degeneration (myopathy)</li> <li>suggests a potential LMN problem (neuropathy)</li> <li>the size of the fibrillations usually directly correspond to the severity of the injury</li></ol>

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86
Q

<p>what are fasciculations?</p>

A

<p>spontaneous, twitch like contraction</p>

<p>not necessarily indivitive of pathology (ex: eye twitch)</p>

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87
Q

<p>what types of disorders/diseases are fasciculations more common with?</p>

A

<ol> <li>a disease involving alpha motor neurons</li> <li>chronic demyelination conditions</li></ol>

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88
Q

<p>what might suggest to you that a fasciculation is normal rather than due to a disease?</p>

A

<p>it is singular in event, not multiple is short succession</p>

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89
Q

<p>what is a complex reptitive discharge (CRD)?</p>

A

<p>polyphasic waveforms with fairly fixed amplitudes that show up in a high but stable discharge rate</p>

<p>sounds like a machine gun</p>

<p>spontaneous discharge of multiple different muscle fibers that are asychonous</p>

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90
Q

<p>what types of conditions are CRDs observed in?</p>

A

<ol> <li>neurogenic</li> <li>myopathic</li> <li>generally observed with chronic conditions</li> <li>hereditory neuropathic diseases</li></ol>

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91
Q

<p>what are Myokymic discharges?</p>

A

<p>groups of recurring spontaneous MUAP that fire in a briefrepetitive burst pattern</p>

<p></p>

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92
Q

<p>what are Myotonic potentials?</p>

A

<p>rhythmic electrical discharges that are arise from muscle fibers all over the place - super spontaneous</p>

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93
Q

<p>what types of disease are myotonic potentials related to?</p>

A

<p>myotonic diseases</p>

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94
Q

<p>an alternative way to group MUAPs observed at rest is by what?</p>

A

<p>whether they fire alone or in groups</p>

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95
Q

<p>what types of MUAPs fire alone at rest?</p>

A

<ol> <li>EPSs</li> <li>Fibrillation potentials</li> <li>Myotonic Discharges</li></ol>

<p></p>

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96
Q

<p>what types of MUAPs fire in groups?</p>

A

<ol> <li>adjacent muscle fibers <ol> <li>CRD</li> <li>insertional activity</li> </ol> </li> <li>motor unit potentials <ol> <li>fasciculation potentials</li> <li>myokymic discharges</li> <li>neurotonic discharges</li> </ol> </li></ol>

<p></p>

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97
Q

<p>how would you describe the shape of a normal MUAP during muscle activation EMG?</p>

A

<ol> <li>biphasic</li> <li>triphasic</li></ol>

<p></p>

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98
Q

<p>when a neurogenic injury occurs, what changes will be observed immediately in an EMG?</p>

A

<p>reduced recruitment</p>

<p>increase in firing rates ofMUAPs</p>

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99
Q

<p>when a neurogenic injury occurs, what changes will be oberved after collateral sprouting has occured?</p>

A

<p>the shape of the MUAP will change from triphasic to polyphasic</p>

<p>(MUAPs will be out of sync)</p>

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100
Q

<p>what are polyphasic MUAPs indicative of?</p>

A

<p>neurogenesis</p>

<p>collateral sprouting has most likely occured following a neurogenic injury and the new branches of the nerves are trying to figure out how to fire in sync again, they are disoriented</p>

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101
Q

<p>after a long time has passed following a neurogenic injury (>6 months) what changes will be observed on an EMG?</p>

A

<p>shape is once again triphasic</p>

<p>amplitude will be greater (1 nerve with 2x as many muscle fibers = must fire at a higher amplitude)</p>

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102
Q

<p>myopathic = decrease in \_\_\_\_\_\_\_\_\_</p>

A

<p>number of viable muscle fibers</p>

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103
Q

<p>what are the 5 primary categories of tests for cognitive status?</p>

A

<ol> <li>consciousness</li> <li>orientation</li> <li>attention/concentration</li> <li>memory</li> <li>executive function</li></ol>

<p></p>

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104
Q

<p>what are the levels of consciousness?</p>

A

<ol> <li>alert/fully conscious</li> <li>lethargy = general slowing of cognitive and motor processes</li> <li>obtundation = dulled/blunted sensitivity, difficult to arouse</li> <li>stupor = semi-conscious state, aroused only w/deep pressure pain</li> <li>coma</li></ol>

<p></p>

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105
Q

<p>what is the gold-standard test for levels ofconsciousness?</p>

A

<p>Glascow Coma Scale (GCS)</p>

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106
Q

<p>what are the 3 areas of consciousness measured in the GCS?</p>

A

<ol> <li>eye opening</li> <li>motor response</li> <li>verbal response</li></ol>

<p>*graded 3-15 (<8 = severe; 9-12 moderate; 13-15 mild)</p>

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107
Q

<p>What are the 3-4 primary areas of examination for orientation?</p>

A

<ol> <li>Person</li> <li>Place</li> <li>Time</li> <li>Situation</li></ol>

<p></p>

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108
Q

<p>what are the 4 different aspects of attention/concentration?</p>

A

<ol> <li>sustained attention</li> <li>selective attention</li> <li>divided attention</li> <li>alternating attention</li></ol>

<p></p>

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109
Q

<p>what is sustained attention?</p>

<p>How can we test it?</p>

A

<p>ability to sustain and focus attention over a duration of time</p>

<p>tested via the Cancellation Test</p>

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110
Q

<p>what is the Cancellation test?</p>

A

<p>a method of testing sustained attention</p>

<p>instruct pt to inspect an image and circle all of the \_\_\_\_\_\_ in the image. Will take a lot of time and require a lot of attention</p>

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111
Q

<p>what is selective attention?</p>

<p>How can we test it?</p>

A

<p>ability to screen and process relevant sensory info about the task and environment while screening out irrelevant info</p>

<p>Test = Stroop Test</p>

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112
Q

<p>what is the Stroop Test?</p>

A

<p>used to test selective attention</p>

<p>look at a letter outloud and say the color of the word rather than the word itself</p>

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113
Q

<p>what is divided attention?</p>

<p>How can we test it?</p>

A

<p>ability to perform 2 tasks simultaneously</p>

<p>Walkie-Talkie Test</p>

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114
Q

<p>what is alternating attention?</p>

<p>How can we test it?</p>

A

<p>attention flexibility</p>

<p>shifting your attention back and forth between 2 different things</p>

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115
Q

<p>What is memory?</p>

A

<p>the capacity to store knowledge, experiences, and perceptions for recall and recognition</p>

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116
Q

<p>what are the 2 types of memory?</p>

A

<p>Declarative (Explict)</p>

<p>Non-declarative (Procedural/Implict)</p>

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117
Q

<p>what is declarative memory?</p>

A

<p>conscious recollection of facts and events</p>

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118
Q

<p>what is non-declarative memory?</p>

A

<p>recall movements/movement schema without conscious recollections</p>

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119
Q

<p>what is another 3 part classification of memory?</p>

A

<ol> <li>immediate recall <ul> <li>"repeat after me" (seconds to minutes)</li> </ul> </li> <li>short-term memory <ul> <li>recent or working memory (minutes to hours/days)</li> </ul> </li> <li>long-term memory <ul> <li>remote memory (months to years)</li> </ul> </li></ol>

<p></p>

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120
Q

<p>What is executive function?</p>

A

<p>capacity to engage successfully in independent, purposeful, self-directed behavior</p>

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121
Q

<p>what are the different aspects of executive function?</p>

A

<ol> <li>volition/planning</li> <li>problem solving/reasoning</li> <li>insight/awareness <ul> <li>poor judgement</li> </ul> </li> <li>social pragmatics <ul> <li>inappropriate behaviors</li> </ul> </li> <li>self-regulation/purposeful action <ul> <li>initiate, maintain, switch, and stop tasks</li> </ul> </li></ol>

<p></p>

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122
Q

<p>what is difference between sensation and perception?</p>

A

<p>sensation = raw data</p>

<p>perception = interpretation of data</p>

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123
Q

<p>what are 2 critera for sensation to occur?</p>

A

<p>adequate arousal and selective attention</p>

<p>adequate stimulus level to activate sensory receptor</p>

<p>*entire pathway must work!</p>

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124
Q

<p>Give a working definition of perception</p>

A

<p>capacity to transform info from the senses and use it to interact appropriately with the environment</p>

<p>selective, integrative, dynamic process that includes problem solving and memory</p>

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125
Q

<p>what type of sensations arecarried in the spinothalamic tract?</p>

A

<ol> <li>pain</li> <li>temperature</li> <li>crude touch</li></ol>

<p></p>

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126
Q

<p>what types of receptors are utilized in the spinothalamic tract?</p>

A

<ol> <li>free nerve endings</li> <li>cutaneous receptors in the skin</li></ol>

<p></p>

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127
Q

<p>what are the afferent fiber characteristics in the spinothalamic tract?</p>

A

<p>small, thin, slow conducting</p>

<p>no myelination</p>

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128
Q

<p>where is the spinothalamic tract heading?</p>

<p>what are it's major connections?</p>

A

<ol> <li>lower brainstem</li> <li>thalamus</li> <li>limbic system</li> <li>diffuse cortical areas</li></ol>

<p></p>

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129
Q

<p>what types of sensations are carried by the dorsal column/medial lemniscus tract?</p>

A

<ol> <li>discriminative touch (tactile location)</li> <li>proprioception</li> <li>kinesthesia</li> <li>vibration</li> <li>2-point discrimination</li></ol>

<p></p>

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130
Q

<p>what types of receptors are utilized in the dorsal column/medial lemniscus tract?</p>

A

<ol> <li>muscle spindle</li> <li>GTOs</li> <li>joint receptors</li> <li>some cutaneous receptors in the skin</li></ol>

<p></p>

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131
Q

<p>what are the afferent fiber types of the dorsal column/medial lemniscus tract?</p>

A

<p>large, thick, rapidly conducting</p>

<p>well myelinated</p>

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132
Q

<p>where is the dorsal column/medial lemniscus tract headed?</p>

A

<p>sensory cortex</p>

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133
Q

<p>what types of sensations are carried in the spinocerebellar tract?</p>

A

<p>"unconscious"</p>

<p>proprioception and kinesthesia</p>

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134
Q

<p>what types of receptors are utilized in the spinocerebellar tracts?</p>

A

<ol> <li>muscle spindles</li> <li>GTOs</li> <li>joint receptors</li> <li>some cutaneous receptors in the skin</li></ol>

<p></p>

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135
Q

<p>what are the afferent fiber types of the spinocerebellar tract?</p>

A

<p>fast, direct, heavily myelinated</p>

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136
Q

<p>where is the spinocerebellar tract headed?</p>

A

<p>cerebellum</p>

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137
Q

<p>What are the 4 major subcategories/components of the perceptual exam?</p>

A

<ol> <li>Body scheme and body image impairments</li> <li>spatial relationships</li> <li>agnosias</li> <li>apraxia</li></ol>

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138
Q

<p>what is the difference between body scheme and body image?</p>

A

<p>body image = visual/mental image of one's body</p>

<p>body scheme = postural model of body (body awareness)</p>

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139
Q

<p>Name a major impairment to body scheme/image</p>

A

<p>Unilateral Neglect</p>

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140
Q

<p>what is unilateral neglect?</p>

A

<p>failure to orient toward, respond to, or report stimuli on the contralateral side to the lesion</p>

<p>*despite normal sensory, visual and motor systems</p>

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141
Q

<p>Unilateral neglect occurs mostly with \_\_\_\_\_\_\_\_ lesions</p>

A

<p>R tempoparietal junction</p>

<p>posterior parietal</p>

<p>(**R side most often)</p>

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142
Q

<p>what are the 2 classification systems for unilateral neglect?</p>

A

<ol> <li>Modality</li> <li>Distribution</li></ol>

<p></p>

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143
Q

<p>what are the 3 types of modality neglect?</p>

A

<ol> <li>sensory</li> <li>motor</li> <li>representational</li></ol>

<p></p>

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144
Q

<p>What is sensory neglect?</p>

A

<p>brain loses ability to maintain awareness of a specific sense as it comes in (can be visual, auditory, or tactile)</p>

<p>the sensation is fine but the perception is off</p>

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145
Q

<p>what is motor neglect?</p>

A

<p>"output neglect"</p>

<p>failure to generate a movement response to a specific stimuli even if the pt. is aware of the stimuli</p>

<p>ex: ball is thrown at you, you only raise 1 arm to catch it even though both arms have 5/5 strength</p>

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146
Q

<p>what is representational neglect?</p>

A

<p>loss of internally generated images</p>

<p>ex: pt asked to recall and draw a clock. They draw a clock with all the numbers on 1 side of a circle</p>

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147
Q

<p>What are the two subcategories of distribution neglect?</p>

A

<ol> <li>Personal</li> <li>Spatial</li></ol>

<p></p>

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148
Q

<p>what is personal neglect?</p>

A

<p>individual lacks awares of entire contralateral side of their body</p>

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149
Q

<p>what is spatial neglect?</p>

A

<p>failure to acknowledge stimuli of the contralateral side of space</p>

<p>can be peripersonal (within reaching space)</p>

<p>extrapersonal (in far space)</p>

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150
Q

<p>Other than unilateral neglect. What are 4 other types of body scheme/body image impairments?</p>

A

<ol> <li>somatoagnosia</li> <li>R-L discrimination</li> <li>vertical disorientation/midline disorientation</li> <li>Pusher syndrome</li></ol>

<p></p>

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151
Q

<p>what is somatoagnosia?</p>

A

<p>an impairment of body scheme</p>

<p>Lack of awareness of relationship of body parts</p>

<p>(how your shoulder relates to your elbow, difficult to differentiate from proprioception)</p>

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152
Q

<p>what portion of the brain is primarily/most often affected with somatoagnosia?</p>

A

<p>usually lesion todominant parietal lobe</p>

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153
Q

<p>what is R-L discrimination?</p>

A

<p>decreased R/L differentiation with body parts and following directions</p>

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154
Q

<p>what portion of the brain is primarily/usually affected with R/L discrimination?</p>

A

<p>lesion to either parietal lobe</p>

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155
Q

<p>what is vertical disorientation/midline disorientation?</p>

A

<p>cannot ID when their body is in the middle</p>

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156
Q

<p>what is Pusher Syndrome?</p>

A

<p>a subtype of vertical/midline disorientation</p>

<p>characterized by leaning and active pushing towards hemiplegic side w/o compensation for instability and with resistance to passive correction towards midline</p>

<p></p>

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157
Q

<p>what portion of the brain is primarily affected with pusher syndrome?</p>

A

<p>lesion to R hemisphere centered in area of posterolateral thalamus</p>

<p>tends to be more common when L hemiplegia is present alongside L spatial and sensory neglect</p>

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158
Q

<p>list the various spatial relationships impairments</p>

A

<ol> <li>Figure ground</li> <li>spatial relations disorder</li> <li>position in space disorder</li> <li>topographical disorientation</li> <li>depth and distance perception</li></ol>

<p></p>

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159
Q

<p>what is Figure ground?</p>

A

<p>the inability to distinguish a figure from the background in which it is embedded</p>

<p>ex: pick a screwdriver out of a toolbox full of tools</p>

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160
Q

<p>what is spatial relations disorder?</p>

A

<p>the inability to percieve relationships of one object in space to another object, or to one's self</p>

<p></p>

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161
Q

<p>what primarily causes spatial relations disorder?</p>

A

<p>lesion in the R inferior parietal lobe</p>

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162
Q

<p>what is position in space disorder?</p>

A

<p>decreased ability to perceive and interpret spatial concepts</p>

<p>can't distinguis between opposite directional/spatial concepts</p>

<p>ex: confused up and down</p>

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163
Q

<p>what is topographical disorientation?</p>

A

<p>difficulty perceiving relationships from one location to another in the environment</p>

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164
Q

<p>what is depth and distance perception?</p>

A

<p>inaccurate judgement of directions, distance, and depth</p>

<p>more broad than spatial relationship disorders, and deals with environmental cues (like difficulty negotiating a curb)</p>

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165
Q

<p>what is the primary cause of depth and distance perception issues?</p>

A

<p>lesion of R or bilateral visual assocaition cortex</p>

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166
Q

<p>what does the general term agnosias mean?</p>

A

<p>decreased ability to recognize stimuli despite intact sensory function.</p>

<p>most commonly associated with damage to temporal lobe</p>

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167
Q

<p>what are the different types of agnosias?</p>

A

<ol> <li>Sensory <ol> <li>visual</li> <li>auditory</li> <li>tactile (asterognosis)</li> </ol> </li> <li>Body scheme <ol> <li>anosognosia</li> <li>somatagonsia</li> </ol> </li></ol>

<p></p>

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168
Q

<p>what is visual agnosia?</p>

A

<p>inability to recognize familiar objects despite normal eye function</p>

<p></p>

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169
Q

<p>what type of lesion normally causes visual agnosia?</p>

A

<p>occipital and temporal lobe (R or L)</p>

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170
Q

<p>what is auditory agnosia?</p>

A

<p>inability to recognize non-speech sounds and discriminate between them</p>

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171
Q

<p>what type of lesion normally causes auditory agnosia?</p>

A

<p>left temporal lobe</p>

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172
Q

<p>what is tactile agnosia (astereognosis)?</p>

A

<p>inabilty to recongize objects when handling them, despite normal tactile sensation</p>

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173
Q

<p>what types of lesions normally causes tactile agnosia?</p>

A

<p>parietal/temporal/occipital association areas (R or L)</p>

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174
Q

<p>what is anosognosia?</p>

A

<p>a severe condition in which an individual does not acknowledge, denies, or lacks awareness of presence/severity of one's deficits</p>

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175
Q

<p>define apraxia</p>

A

<p>impairment of voluntary, skilled, well-learned movement</p>

<p>w/o deficits in motor function, sensory function, or coordination</p>

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176
Q

<p>what are the 2 types of apraxia?</p>

A

<p>ideomotor</p>

<p>ideational</p>

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177
Q

<p>what is ideomotor apraxia?</p>

A

<p>breakdown between concept (idea) and performance (motor execution)</p>

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178
Q

<p>what is ideational apraxia?</p>

A

<p>failure in the conceptualization of the task</p>

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179
Q

<p>what type of lesion normally causes apraxia?</p>

A

<p>left frontal or parietal lobes</p>

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180
Q

<p>what is an Upper Motor Neuron (UMN)?</p>

A

<p>descending axons from cortex to brainstem</p>

<p>OR</p>

<p>from brainstem to spinal cord</p>

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181
Q

<p>what is a Lower Motor Neuron (LMN)?</p>

A

<p>axons exiting the CNS and innervating peripheral nerves</p>

<p>motor divisions of cranial nerves</p>

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182
Q

<p>is weakness a sign of an UMN or LMN Lesion?</p>

A

<p>Both</p>

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183
Q

<p>is atrophy a sign of an UMN or a LMN lesion?</p>

A

<p>LMN lesion</p>

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184
Q

<p>are fasiculations a sign of an UMN or LMN lesion?</p>

A

<p>LMN</p>

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185
Q

<p>are increased reflexes a sign of an UMN or a LMN lesion?</p>

A

<p>UMN lesion</p>

<p>(LMN have decreased reflexes)</p>

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186
Q

<p>is decreased tone a sign of an UMN or a LMN lesion?</p>

A

<p>LMN lesion</p>

<p>(increased tone = UMN lesion)</p>

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187
Q

<p>What are the 6 components of the whole clinical neurological exam?</p>

A

<ol> <li>Mental Status</li> <li>Cranial Nerves</li> <li>Motor Exam</li> <li>Sensory Exam</li> <li>Reflexes</li> <li>Coordination/Gait</li></ol>

<p></p>

188
Q

<p>Which cranial nerves are pure sensory nerves?</p>

A

<ol> <li>Olfactory (CN 1)</li> <li>Optic (CN 2)</li> <li>Auditory (CN 8)</li></ol>

<p></p>

189
Q

<p>which cranial nerves are pure motor nerves?</p>

A

<ol> <li>Trochlear (CN 4)</li> <li>Abducent (CN 6)</li> <li>Accessory (CN 11)</li> <li>Hypoglossal (CN 12)</li></ol>

<p></p>

190
Q

<p>which cranial nerves are mixed nerves (both motor and sensory)?</p>

A

<ol> <li>Trigeminal (CN 5)</li> <li>Facial (CN 7)</li> <li>Glossopharyngeal (CN 9)</li> <li>Vagus (CN 10)</li> <li>Occulomotor (CN 3)</li></ol>

191
Q

<p>Th test for olfaction (CN 1) includes what 2 tests?</p>

A

<ol> <li>Tests for discrimination (contrast odors)</li> <li>Tests for arousal (noxious stimulant)</li></ol>

<p></p>

192
Q

<p>T/F: the CN 1 test is not often included in the cranial nerve screen</p>

A

<p>TRUE</p>

<p>this nerve tends to be spared from a lot of issues unless there is a specific pathology that impacts this sense</p>

193
Q

<p>If a patient presents with unilateral or bilateral loss of smell but can still distinguish the smell what is the differential diagnosis?</p>

A

<p>a local nasal disease rather than a neural condition</p>

194
Q

<p>When testing CN 1, what would suggest to you that there might be a neural pathology invovled?</p>

A

<p>if the pt has a distorted sense of smell for a neutral scent</p>

195
Q

<p>List some possible mechanisms of injury to the olfactory nerve</p>

A

<ol> <li>Parkinson's disease</li> <li>chronic meningeal inflammation</li> <li>tumors in sub frontal region</li> <li>head injuries</li> <li>heavy smoking</li></ol>

<p></p>

196
Q

<p>What tests are included in the CN 2 exam?</p>

A

<ol> <li>Visual acuity</li> <li>Color discrimination</li> <li>Field Cuts</li> <li>Pupillary response to light accommodation</li> <li>Visual Extinction</li></ol>

<p></p>

<p></p>

197
Q

<p>What is visual acuity? How do we test it?</p>

A

<p>ability to see clearly</p>

<p>Snellin chart</p>

198
Q

<p>What is a visual field cut?</p>

A

<p>blindness in one of the 4 quadrants of the eye</p>

<p>this is due to damage to the optic nerve and is NOT the same as visual neglect</p>

199
Q

<p>What is the visual extinction test?</p>

A

<p>a visual neglect test</p>

<p>helpful to include in testing the optic nerve and ruling out visual neglect over a visual field cut</p>

200
Q

<p>what cranial nerves are responsible for innervating the extraoccular muscles?</p>

A

<p>CN III<br></br>CN IV</p>

<p>CN VI</p>

201
Q

<p>CN III innervates extraoccular muscles that perform what movements?</p>

A

<p>elevation</p>

<p>depression</p>

<p>ADDuction</p>

<p>(PSNS: pupil constriction - efferent limb of pupillary reflex)</p>

202
Q

<p>CN IV innervates extraoccular muscles that perform what movements?</p>

A

<p>Depression/intorsion</p>

203
Q

<p>CN VI innervates extraoccular muscles that perform what movements?</p>

A

<p>ABDuction</p>

204
Q

<p>what test is performing the examination of CN 3, 4, and 6?</p>

A

<p>Big H test</p>

205
Q

<p>if a patient presents with a gaze palsy in which both eyes are skewed in the same direction, what type of lesion are you suspecting?</p>

A

<p>UMN Lesion</p>

<p>(both eyes have dysconjugate gaze)</p>

206
Q

<p>if a pt presents with a gaze palsy in which both eyes are dysconjugate but are skewed in different directions, what lesion do you suspect?</p>

A

<p>LMN lesion</p>

207
Q

<p>if a pt presents with a gaze palsy in which only one eye has a dysconjugate gaze in a specific direction, what type of lesion are you suspecting?</p>

A

<p>LMN lesion</p>

208
Q

<p>The trigeminal nerve is a mixed sensory and motor nerve. What afferent/efferent info does it carry?</p>

A

<p>Afferent:</p>

<ol> <li>pain</li> <li>temperature</li> <li>joint position</li> <li>vibration</li> <li>anterior 2/3 tongue (somatosensory)</li> <li>nasal sinuses</li></ol>

<p>Efferent</p>

<ol> <li>muscles of mastication</li> <li>tensor tympani</li></ol>

<p></p>

209
Q

<p>How would you test the trigeminal nerve?</p>

A

<ol> <li>Light tough to face <ul> <li>for all branches (V1, 2, 3)</li> </ul> </li> <li>Bite strength <ul> <li>for muscles of mastication</li> </ul> </li> <li>Corneal reflex <ul> <li>tests both V and VII</li> </ul> </li></ol>

210
Q

<p>when is the corneal reflex test most often performed?</p>

A

<p>if a pt is obtunded</p>

<p>not commonly performed if a pt is alert</p>

211
Q

<p>the facial nerve is a mixed sensory and motor nerve. What are it's afferent and efferent branches?</p>

A

<p>afferent</p>

<ol> <li>taste afferents for anterior 2/3 of tongue</li> <li>somatosensory for proprioception of facial muscles</li> <li>somatosensory for skin sensation of posterior ear and external auditory meatus</li> <li>motor for facial expression muscles</li> <li>autonomic motor to lacrimal and salivary glands</li></ol>

<p></p>

212
Q

<p>What is/are the methods for testnig CN VII?</p>

A

<ol> <li>Observation</li> <li>Motor <ol> <li>smile, raise eyebrows, puff out cheeks, purse lips, close eyes tightly</li> </ol> </li> <li>Sensory <ol> <li>taste (not typically done)</li> <li>secretomotor function</li> </ol> </li> <li>Reflexes <ol> <li>corneal reflex (CN V and VII)</li> <li>nasopalpebral reflex</li> </ol> </li></ol>

<p></p>

213
Q

<p>why is taste not typically tested specifically?</p>

A

<p>pts wil often complain about it and will let you know if they have lose some taste</p>

214
Q

<p>what is theformal way to test the salivary glands?</p>

A

<p>give the pt something spicy and then compare the either side of the inside of their mouth.</p>

<p>look for saliva secretion either side</p>

215
Q

<p>When testing CN 7 how can you distinguish between an UMN and a LMN lesion?</p>

A

<p>look at the forehead</p>

<p>UMN = intact forehead muscle function</p>

<p>LMN = entire side of face will lose motor function</p>

216
Q

<p>how is CN IX assessed/tested?</p>

A

<p>Palatal activation</p>

<p>inspect for symmetry→ with a lesion, one side will deviate to uninvolved side</p>

<p>Gag reflex (sensory limb)</p>

217
Q

<p>The gag reflex tests which cranial nerves?</p>

A

<p>CN IX (sensory afferent limb)</p>

<p>CN X (motor efferent limb)</p>

218
Q

<p>how would you expect a pt with CN 9 and 10 dysfunction to sound?</p>

A

<p>hoarse</p>

<p>difficulty with speech production</p>

219
Q

<p>how is CN 11 assessed?</p>

A

<p>Shoulder Shrug (UTrap)</p>

<p>Side bend and rotate (SCM)</p>

220
Q

<p>how would an UMN lesion impact CN 11?</p>

A

<p>pt will present with trapezius weakness</p>

<p>BUT the SCM will be spared</p>

221
Q

<p>how would a LMN lesion impact CN 11?</p>

A

<p>both the trapezius and SCM would be impacted</p>

222
Q

<p>how is CN 12 assessed?</p>

A

<p>Stick out tongue (tongue protrusion)</p>

<p>direction may indicate UMN vs LMN</p>

223
Q

<p>how will a pt present with an UMN lesion of CN 12?</p>

A

<p>tongue will deviate <u><strong>away </strong></u>from the side of the lesion</p>

<p>(picture on the right)</p>

224
Q

<p>how will a pt present with a LMN lesion of CN 12?</p>

A

<p>tongue will deviate <u><strong>toward </strong></u>the side of the lesion</p>

<p>atrophy and fasciculations will also be observed</p>

<p>(left picture)</p>

225
Q

<p>T/F: you can performm the motor exam part of the clincial neurological exam without even toughing the pt?</p>

A

<p>TRUE</p>

226
Q

<p>what are the components of the Motor Exam?</p>

A

<ol> <li>Inspection at rest</li> <li>Task Based observation</li> <li>Tone assessment</li> <li>MMT</li></ol>

<p></p>

227
Q

<p>what are you looking for during the inspection at rest portion of the Motor Exam?</p>

A

<ol> <li>Muscle atrophy</li> <li>Fasiculation</li> <li>Hypertrophy</li> <li>Tremors</li> <li>Involuntary movements</li> <li>posturing</li></ol>

<p></p>

228
Q

<p>What is posturing?</p>

A

<p>occurs when a pt picks up a very specific position of their UE and LE base don where their inujury was</p>

229
Q

<p>What are the 2 main kinds of posturing?</p>

A

<ol> <li>Decorticate posture</li> <li>Decerebrate posture</li></ol>

<p></p>

230
Q

<p>Describe decorticate posture</p>

A

<p>pt has full flexion of the UE and they hold it there</p>

<p>full extension of LE</p>

<p></p>

231
Q

<p>What type of damage would result in decorticate posturing?</p>

A

<p>damage to brainstemm above the red nucleus</p>

232
Q

<p>Describe decerebrate posture</p>

A

<p>pt has full extension of UE and LE</p>

<p>might still have some finger flexion</p>

233
Q

<p>What type of damage would result in decerebrate posture?</p>

A

<p>damage underneath/lower than the red nucleus in the brainstem</p>

<p>ex: pontine lesion</p>

234
Q

<p>T/F: posturing has no prognostic value</p>

A

<p>FALSE</p>

<p>it is an indicator that the pt might not progress/get that much better</p>

235
Q

<p>What is the distinction between the tone assessment and MMT?</p>

A

<p>tone assessment = resitance against passive movement</p>

<p>MMT = greater resistance, helps ID patterns of weakness</p>

236
Q

<p>What is assessedduring the Sensory Exam?</p>

A

<ol> <li>Pain</li> <li>Temperature</li> <li>Vibration</li> <li>Proprioception</li> <li>Light touch/2 pt discrimination</li></ol>

237
Q

<p>How are reflexes graded?</p>

A

<p>0-5</p>

<p>0 = absent</p>

<p>1 = trace</p>

<p>2 = normal</p>

<p>3= brisk</p>

<p>4 = non-sustained clonus</p>

<p>5 = sustained clonus</p>

238
Q

<p>If reflexes are abnormally increased this is indicative of what?</p>

A

<p>UMN lesion</p>

239
Q

<p>if reflexes are abnormally decreased, this is indicative of what?</p>

A

<p>LMN lesion</p>

<p>but could be muscle, nerve fiber and NMJ</p>

240
Q

<p>What are some primary neuromusclar impairments that can result from a neurological pathology?</p>

A

<ol> <li>Muscle weakness</li> <li>Abnormal tone</li> <li>Coordination deficits</li> <li>involuntary movements</li></ol>

<p></p>

241
Q

<p>What are some secondary neuromusclar impairments that can result from a neurological pathology like an UMN lesion?</p>

A

<ol> <li>ROM and alignment issues</li> <li>Endurance issues</li> <li>Pain</li></ol>

<p></p>

242
Q

<p>how would you define muscle weakness as a neuromusclar impairment?</p>

A

<p>inability to generate force or recruit/modulate motor units</p>

243
Q

<p>list some neural contributions that can result in the primary neuromusclar impairment of muscle weakness</p>

A

<p>Change in:</p>

<ol> <li># of motor units recruited</li> <li>D/C frequency</li> <li>type of motor unit recruited</li></ol>

<p></p>

244
Q

<p>What are some potential neurological pathologies that can result in neuromusclar weakness as an impairment?</p>

A

<ol> <li>Cortical lesions</li> <li>lesions in descending pathways</li> <li>disruption of impulses to alpha motor neurons</li> <li>peripheral nerve injury</li> <li>synaptic dysfunction at NMJ</li></ol>

<p></p>

245
Q

<p>Muscle weakness as a neurological impairment can result in what secondary impairments/observations?</p>

A

<ol> <li>postural abnormalities</li> <li>asymmetrical weight bearing</li> <li>abnormal synergies</li></ol>

<p></p>

246
Q

<p>list 2 types of abnormal synergies</p>

A

<ol> <li>Flexor synergy (UE)</li> <li>Extensor synergy (LE)</li></ol>

<p></p>

247
Q

<p>describe a flexory synergy?</p>

A

<p>scapular retraction and elevation</p>

<p>shoulder abduction and ER</p>

<p>elbow flexion</p>

<p>supination</p>

<p>wrist and finger flexion</p>

248
Q

<p>describe an extensor synergy</p>

A

<p>hip extension, adduction and IR</p>

<p>knee extension</p>

<p>ankle PF and inversion</p>

<p>toe PF</p>

249
Q

<p>what is tone?</p>

A

<p>muscles' resistance to passive stretch</p>

250
Q

<p>Describe the continuum/varying levels of tone</p>

A

<p>From too little to too much</p>

<ol> <li>Flaccid</li> <li>Hypotonicity</li> <li>normal</li> <li>hypertonic/spasticity</li> <li>Rigid</li></ol>

251
Q

<p>what are the neural contributions to normal tone?</p>

A

<p>net balance of descending input on motor neurons from:</p>

<p>corticospinal tracts</p>

<p>rubrospinal tracts</p>

<p>reticulospinal tracts</p>

<p>vestibulospinal tracts</p>

<p>as well as the sensitivity of synaptic connections</p>

252
Q

<p>what are the non neural contributions to normal tone?</p>

A

<ol> <li>CT plasticity</li> <li>viscoelastic properties of the muscles, tendons, and joints</li></ol>

<p></p>

253
Q

<p>How is spasticity different from hypertonia?</p>

A

<p>spasticity is velocity dependent and hypertonia is not</p>

254
Q

<p>Spasticity can sometime be described as a \_\_\_\_\_\_\_\_\_\_\_</p>

A

<p>clasp-knife phenomenon</p>

255
Q

<p>what is a typical cause of spasticity and a common result/association?</p>

A

<p>damage to pyramidal tract or other nearby descending paths</p>

<p>can be associated with clonus (commonly in distal > proximal extremities)</p>

256
Q

<p>Describe the mechanism by which spasticity occurs</p>

A

<ol> <li>changes in neural contributions</li> <li>results in decreased descending activity</li> <li>reduction of inhibitory synaptic input</li> <li>increases tonic excitatory input</li> <li>results in alterations to threshold of stretch reflex</li></ol>

257
Q

<p>List 2 scales typically used to measure tone</p>

A

<ol> <li>Modified Ashworth Scale</li> <li>Tardieu scale</li></ol>

<p></p>

258
Q

<p>which scale used to measure tone, also gives us info on spasticity?</p>

A

<p>Tardieau</p>

<p>since we vary the velocities (V1, 2, 3)</p>

259
Q

<p>which applied velocities equate to spasticity on the Tardieau scale?</p>

A

<p>V2 = speed of limb falling under gravity</p>

<p>V3 = fast as possible</p>

260
Q

<p>In what muscle group is hypertonia typically observed?</p>

A

<p>Flexors</p>

261
Q

<p>When testing hypertonia with movements, it can be described as \_\_\_\_\_\_\_\_\_ or \_\_\_\_\_\_\_\_\_</p>

A

<p>leadpipe or cogwheel</p>

262
Q

<p>what is the difference between leadpipe and cogwheel hypertonia?</p>

A

<p>leadpipe = constant resistance to movements throughotu entire ROM</p>

<p>Cogwheel = alternating episodes of resistance and relaxation</p>

263
Q

<p>what is hypertonia at rest called?</p>

A

<p>Posturing</p>

264
Q

<p>What are the 2 types of posturing?</p>

A

<p>decorticate = UE flexion, LE extension/IR/PF</p>

<p>decerebrate = UE and LE extension</p>

265
Q

<p>what type of posturing is due to a lesion at or above the level of the red nucleus?</p>

A

<p>decorticate posturing</p>

266
Q

<p>characteristic of the tone abnormality depends on what factors?</p>

A

<ol> <li>type and location of pathology</li> <li>Chronicity <ul> <li>increases in nonneural changes = increased "stiffness"</li> </ul> </li></ol>

<p></p>

267
Q

<p>List the type of abnormal tone that would result if a lesion occured at the cortical, brainstem, and basal ganglia level?</p>

A

<ol> <li>cortical: pyramidal → change in descending inputs of alpha motor neurons→ spasticity</li> <li>Basal ganglia: extra pyramidal→ rigidity</li> <li>brainstem: above/below red nucleus→ decorticate/decerebrate posturing</li></ol>

<p></p>

268
Q

<p>List some pathologies in which hypertonicity is commonly observed</p>

A

<ol> <li>CVA</li> <li>TBI</li> <li>MS</li> <li>Parkinsons Disease (rigidity)</li></ol>

269
Q

<p>define hypotonicity</p>

A

<p>reduction in resistance to lengthening</p>

<p>reduction in "stiffness"</p>

270
Q

<p>hypotonicity can be described as \_\_\_\_\_\_\_ or \_\_\_\_\_\_\_</p>

A

<p>floppy = collapse into gravity, harder to excite</p>

<p>flaccidity = complete loss of muscle tone</p>

271
Q

<p>what causes hypotonicity?</p>

A

<p>disruption of afferent input from stretch reflex→</p>

<p>lack of cerebellar efference influence→</p>

<p>result in decreased input to gamma motor neurons</p>

272
Q

<p>List some pathologies where hypotonicity is commonly observed</p>

A

<ol> <li>Cerebellar lesions</li> <li>down syndrome</li> <li>musclar dystrophies</li> <li>late stage ALS</li> <li>post-polio</li> <li>Acute CNS injuries→ typically end up resulting in hypertonicity/spasticity once subactue phase is over</li></ol>

<p></p>

273
Q

<p>what are the functional implications for increased tone?</p>

A

<ol> <li>abnormal posturing</li> <li>misalignment</li> <li>high risk for injury during prolonged rest (skin breakdown)</li> <li>bias with recruitment <ol> <li>increased likelihood of synergistic movement</li> </ol> </li> <li>destabilization with changes in position (clonus, increased risk for contractures)</li></ol>

<p></p>

274
Q

<p>what are the functional implications for decreased tone?</p>

A

<ol> <li>fall into gravity</li> <li>high risk for injury during dynamic tasks</li></ol>

<p></p>

275
Q

<p>define coordination</p>

A

<p>ability to use parts of the body together smoothly and efficiently</p>

276
Q

<p>what are the critical components of coordination?</p>

A

<ol> <li>sequencing</li> <li>timing</li> <li>grading</li></ol>

<p></p>

277
Q

<p>define incoordination</p>

A

<p>movements that are awkward, uneven, inaccurate</p>

<p>disrupting of sequencing, timing and grading</p>

<p>loss of coupling between synergistic joints and muscles</p>

278
Q

<p>incoordination is typically observed with what types of lesions?</p>

A

<p>motor cortex</p>

<p>basal ganglia</p>

<p>cerebellar</p>

<p>(proprioceptive lesions too)</p>

279
Q

<p>the functional implications of incoordination can be divided into what categories?</p>

A

<ol> <li>grading/scaling dysfunction</li> <li>timing difficulties</li> <li>activation and sequencing problems</li></ol>

<p></p>

280
Q

<p>what are the types of grading/scaling dysfunctions found with incoordination?</p>

A

<ol> <li>dysmetria = under/overshooting intended position (a type of ataxia)</li> <li>hypermetria = moving beyond intended goal</li> <li>hypometria = moving short of intended goal</li></ol>

<p></p>

281
Q

<p>list some timing difficulties that are a result of incoordination</p>

A

<ol> <li>increased reaction times</li> <li>slowed movement times</li> <li>difficulty terminating movements</li> <li>rebound phenomenon</li> <li>dysdiadochokinesia</li></ol>

<p></p>

282
Q

<p>list some activation and sequencing problems that occur with incoordination</p>

A

<ol> <li>abnormal synergies</li> <li>coactivation</li> <li>impaired inter-joint coordination</li></ol>

<p></p>

283
Q

<p>what are the components of the coordination examination?</p>

A

<ol> <li>finger to nose</li> <li>alternating pronation/supination</li> <li>hand or foot tapping</li> <li>heel to shin</li></ol>

<p></p>

<p></p>

284
Q

<p>List several categories/types of involuntary movements that are primary neuromusclar impairments</p>

A

<ol> <li>dystonia</li> <li>tremors</li> <li>choreiform</li> <li>athetosis</li></ol>

<p></p>

285
Q

<p>what is dystonia?</p>

A

<p>syndrome dominated by sustained muscle contractions</p>

<p>causing twisting, repetitive movements, and abnormal postures</p>

286
Q

<p>what region of the brain is dystonia correlated with?</p>

A

<p>basal ganglia</p>

287
Q

<p>what are tremors?</p>

A

<p>rhythmic, involuntary oscillatory movement of a body part</p>

<p>can be intermittent or constant, sporadic or as a sequale to a disease or injury</p>

288
Q

<p>what is the difference between a resting and active tremor?</p>

A

<p>resting = occurs in a body part that is not voluntarily activated (it's relaxed)</p>

<p>active = any tremor produced by voluntary contraction of muscle (can be postural or intention)</p>

289
Q

<p>what is a postural tremor? Intention tremor?</p>

A

<p>postural = person maintains a part of body against gravity</p>

<p>intention = produced with purposeful movement</p>

290
Q

<p>what is a choreiform?</p>

A

<p>involuntary, rapid, irregular and jerky movements</p>

<p>seen with Huntingtons disease and is a SE of PD meds</p>

291
Q

<p>what is athetosis?</p>

A

<p>slow, writhing and twisting movements</p>

<p>UE > LE</p>

<p>common in CP</p>

292
Q

<p>What causes endurance issues to be a secondary neuromuscular impairment?</p>

A

<ol> <li>decrease in central drive to spinal cord motor neurons</li> <li>decrease in activity level/immobility</li></ol>

293
Q

<p>T/F: There is a greater proportion of our brain devoted to vision than any other sense?</p>

A

<p>TRUE</p>

<p>multiple concurrent visual processes are ongoing continuously like:</p>

<ol> <li>conscious perception of visual image info</li> <li>conventional visual reflexes</li> <li>saccadic movements</li> <li>regulation of sleep/wake</li></ol>

<p></p>

294
Q

<p>A lesion to the optic nerve prior to the optic chiasm would result in what type of visual deficit?</p>

A

<p>blindness in the ipsilateral eye</p>

295
Q

<p>what are the functional implications to ipsilateral blindness?</p>

A

<ol> <li>poor depth perception</li> <li>small visual field</li> <li>far peripheral vision is impacted = difficulty with driving and other higher level tasks</li> <li>potential musculoskeletal issues like pain from positioning to compensate</li></ol>

<p></p>

296
Q

<p>compression of the optic chiasm would result in what visual defict?</p>

A

<p>binasal hemianopsia = loss of nasal fields bilaterally, temporal fields spared</p>

297
Q

<p>what are the functional implications of binasal hemianopsia?</p>

A

<p>trouble with near vision and any tasks that utilize that like reading</p>

<p>difficulty concentrating</p>

<p>difficulty with ADLS</p>

<p>**these pts can usually learn to compensate pretty well though</p>

298
Q

<p>a lesion to the optic chiasm would result in what visual deficit?</p>

A

<p>bitemporal hemianopsia = results in loss of temporal fields, nasal fields spared</p>

<p></p>

299
Q

<p>bitemporal hemianopsia is commonly seen with what type of injury?</p>

A

<p>pituitary tumors</p>

300
Q

<p>what are the functional implications of bitemporal hemianopsia?</p>

A

<p>it's like having horse blinders on!</p>

<p>miss peripheral objects and trip on things</p>

<p>miss doors</p>

<p>common fall risk</p>

301
Q

<p>what do patients with bitemporal hemianopsia require?</p>

A

<p>prism glasses or other external aids to be safe on their feet</p>

<p></p>

302
Q

<p>a lesion to the optic tract after the optic chiasm results in what type of visual deficit?</p>

A

<p>homonymous hemianopsia = complete loss in affected region of binocular visual field</p>

<p></p>

<p>Temporal half of R/L visual field + nasal half of L/R visual field</p>

303
Q

<p>homonymous hemianopsia is common with what type of injury?</p>

A

<p>CVA</p>

304
Q

<p>what are the functional implications of homonymous hemianopsia?</p>

A

<p>difficulty seeing everything on one side</p>

<p>must teach pt to turn towards the side they are missing</p>

305
Q

<p>a lesion to the lower division of the optic radiations (in temporal lobe) results in what visual deficit?</p>

A

<p>upper quadrantopia</p>

306
Q

<p>what are the functional implications for someone with upper quadratanopia?</p>

A

<p>none really!</p>

<p>just mostly annoying to pts but they can function just fine</p>

307
Q

<p>a lesion to the upper division of the optic radiation (temporal lobe) would result in what visual deficit?</p>

A

<p>lower quadrantanopia</p>

308
Q

<p>what are the functional implications of lower quadrantanopia?</p>

A

<p>might just be an annoyance and pt can function/adapt just fine</p>

<p>BUT, pts often forget to compensate with this making tripping and falling more common</p>

309
Q

<p>what causes homonymous hemianopia with macular sparring?</p>

A

<p>a lesion to both division of the optic radiations</p>

<p>or a lesion to the visual cortex</p>

310
Q

<p>what are the functional implications to homonymous hemianopsia with maccular sparring?</p>

A

<p>the exact same as homonymous hemianopsia</p>

311
Q

<p>what is the typical cause of monoaural hearing loss?</p>

A

<p>peripheral lesion/damage</p>

<p>cochlear lesion or damage to CN VIII</p>

312
Q

<p>what does having 2 ears help us with?</p>

A

<p>localization of source of sound</p>

313
Q

<p>what are some common causes of acquired hearing loss?</p>

A

<ol> <li>acoustic neuroma</li> <li>meniere's disease</li> <li>traumatic brain injury</li> <li>ototoxicity</li> <li>presbycusis</li></ol>

<p></p>

314
Q

<p>what are the functional implications of hearing loss?</p>

A

<p>can impact the ability to participate in social settings</p>

<p>but other than that none really/just annoying</p>

315
Q

<p>T/F: if there is acquired hearing loss, vestibular loss/dysfunction is usually not far behind</p>

A

<p>TRUE</p>

316
Q

<p>List the 3 vestibularreflexes</p>

A

<ol> <li>Vestibulo-occular reflex (VOR)</li> <li>Vestibulospinal reflex (VSR)</li> <li>Vestibulocollic reflex (VCR)</li></ol>

<p></p>

317
Q

<p>what is the VOR?</p>

A

<p>allows us to stabilize gaze during head movements</p>

<p>results in eye movements that equally coutner head movements</p>

318
Q

<p>describe how the VOR would work with L head turning</p>

A

<p>+L semicircular canals→ +R abducens and +L occulomotor to move eyes</p>

<p></p>

<p>-R semicircular canals→ -L abducens and -R occulomotor</p>

319
Q

<p>Vestibular damage involving the VOR would most likely impact what structures?</p>

A

<ol> <li>Central: damage to midbrain and pons</li> <li>Peripheral: CN VIII, labryinth structures</li></ol>

<p></p>

320
Q

<p>damage to the VOR would result in what impairments?</p>

A

<ol> <li>difficulty stabilizing image on retina while head is moving</li> <li>bilateral vestibular dysfunction <ol> <li>oscillopsia = bouncing vision</li> </ol> </li> <li>unilateral vestibular dysfunction <ol> <li>nystagmus</li> <li>saccedes</li> </ol> </li></ol>

<p></p>

321
Q

<p>what do the VSR and VCR help with?</p>

A

<p>postural adjustments</p>

<p></p>

322
Q

<p>what structures are involved with the VSR?</p>

A

<ol> <li>otoliths (utricle and saccule) project to LVN</li> <li>axons descend to antigravity muscles at all levels of the spinal cord</li></ol>

<p></p>

323
Q

<p>what structures are involved with the VCR?</p>

A

<ol> <li>MVN axons descend in MLF to upper cervical levels of spinal cord <ul> <li>these help dictate head position in response to head rotation</li> </ul> </li></ol>

<p></p>

324
Q

<p>how does the VSR work?</p>

A

<p>Head is tilted to one side</p>

<ol> <li>Canals and otoliths are stimulated ipsilaterally (and inhibited contralateral)</li> <li>Increased input through the vestibular nerve to the vestibular nuclei ipsilaterally</li> <li>Impulses transmitted through the lateral &amp; medial vestibulospinal tracts to the spinal cord</li></ol>

<p>** result in increased lateral extension of trunk on side of head tilt, increased flexion contralaterally</p>

325
Q

<p>Damage to the VSR/VCR would result in what?</p>

A

<p>Postural instability, difficulty sensing falling/tipping</p>

<p>Truncal ataxia</p>

326
Q

<p>what is truncal ataxia?</p>

A

<p>incoordination, unstable trunk movement during movement</p>

327
Q

<p>what is the difference between unimodal and heteromodal corticies?</p>

A

<p>both are association corties</p>

<p>unimodal are modality specific</p>

<p>heteromodal are higher-order functioning</p>

328
Q

<p>what is one reason for hemispheric specialization?</p>

A

<p>a reduction in the amount of time it would take to have both hemisphere's "talk to each other" to accomplish the task</p>

329
Q

<p>T/F: there is bilateral representation of language centers in many right handers?</p>

A

<p>FALSE<br></br>it is observed in 60-70% of LEFT handers</p>

330
Q

<p>what is our non-dominant hemisphere primarily responsible for?</p>

A

<ol> <li>complex visual-spatial skills</li> <li>imparting emotional significance to events and language</li> <li>music perception</li></ol>

<p></p>

331
Q

<p>List some clinical features of a non-dominant hemisphere lesion</p>

A

<ol> <li>visual-spatial analysis/constructional difficulties</li> <li>Gestalt difficulties</li> <li>tendency toward relatively severe personality and emotional changes</li> <li>increased likelihood to have delusions and hallucinations (when compared to the dominant hemisphere)</li></ol>

<p></p>

332
Q

<p>what is meant by constructional difficulties?</p>

A

<p>difficulty judging or matching orientation of lines displayed at different angles</p>

<p>(this person would have a hard time drawing more complex shapes but could draw simple ones)</p>

333
Q

<p>what are gestalt difficuties?</p>

A

<p>overall spatial arrangement difficulties</p>

<p>(a pt would have difficulty understanding how everything is organized in their visual field, ie. big picture)</p>

334
Q

<p>List some odd nondominant syndromes</p>

A

<ol> <li>capgas syndrome</li> <li>fregoli syndrome</li> <li>reduplicative paramnesia</li></ol>

335
Q

<p>what is capgas syndrome?</p>

A

<p>patient insists that their friends and family members have been replaced by identical-looking imposters</p>

336
Q

<p>what is fregoli syndrome?</p>

A

<p>patients belive that different people are actually the same person in disguise</p>

337
Q

<p>what is reduplicative paramnesia?</p>

A

<p>patient believes that a person, place, or object exists as two identical copies</p>

338
Q

<p>List some dominant (usually left) hemisphere functions</p>

A

<ol> <li>Language</li> <li>skilled motor function (praxis)</li> <li>Arithmetic: sequential and analytical calculating skills</li> <li>Musical ability: sequential and analytical skills in trained muscians</li> <li>Sense of directions: following a set of written directions in sequence</li></ol>

<p></p>

339
Q

<p>List some non-dominant (usually right) hemisphere functions</p>

A

<ol> <li>Prosody (emotion conveyed by tone of voice)</li> <li>visual-spatial analysis and spatial attention</li> <li>arithmetic: ability to estimate quantity and to correctly line up columns of numbers on the page</li> <li>musical ability: in untrained musicians, and for complex musical pieces in trained musicians</li> <li>sense of direction: finding one's way by overall sense of spatial orientation</li></ol>

<p></p>

340
Q

<p>how do Broca's and Wernicke's area communicate?</p>

A

<p>arcuate fasciculus</p>

341
Q

<p>List all the regions of the brain associated with language</p>

A

<ol> <li>inferior lateral primary motor cortex</li> <li>Frontal lobes</li> <li>supramarginal gyrus and angular gyrus</li> <li>visual cortex, visual association cortex</li> <li>Non-dominant hemisphere is also involved</li> <li>subcotical regions</li></ol>

<p></p>

342
Q

<p>what is the role of the Frontal Lobe with respect to language processing?</p>

A

<ol> <li>higher-order motor aspects of speech formation and planning</li> <li>syntax</li></ol>

<p></p>

343
Q

<p>what is the role of the supramarginal and angular gyrus (parietal and tempral lobes) in language?</p>

A

<ol> <li>lexicon</li> <li>writing</li></ol>

<p></p>

344
Q

<p>what is the role of the visual and visual association cortices in language?</p>

A

<p>reading</p>

345
Q

<p>List some syndromes related to aphasia</p>

A

<ol> <li>Alexia</li> <li>Agraphia</li> <li>Alexia with agraphia</li></ol>

<p></p>

346
Q

<p>what is alexia?</p>

A

<p>an impairment in reading ability</p>

<p></p>

347
Q

<p>what is agraphia?</p>

A

<p>impairment in writing ability</p>

348
Q

<p>alexia without aphasia will have a lesion where?</p>

A

<p>dominant occipital cortex extending to the posterior corpus callosum (often PCA infarct)</p>

349
Q

<p>Agraphia without aphasia will often involve a lesion where?</p>

A

<p>lesion of inferior parietal lobule of language-dominant hemisphere</p>

350
Q

<p>what is alexia with agraphia?</p>

<p>what regions of the brain does it impact?</p>

A

<p>aphasia absent or only mild dysnomia and paraphasias</p>

<p>lesions of dominant inferior parietal lobe, region of angular gyrus</p>

351
Q

<p>what are the symptoms of gerstmann's syndrome?</p>

A

<ol> <li>agraphia</li> <li>acalculia</li> <li>R/L disorientation</li> <li>Finger agnosia</li></ol>

<p></p>

352
Q

<p>a lesion to what region of the brain often results in gerstmann's syndrome?</p>

A

<p>dominant inferior parietal lobe</p>

<p>(right where the angular gyrus is)</p>

353
Q

<p>List some disorders involving the primary visual cortex</p>

A

<ol> <li>Cortical blindness</li> <li>Blindsight</li> <li>Anton's Syndrome</li></ol>

<p></p>

354
Q

<p>What is cortical blindness?</p>

A

<p>complete visual loss on confrontation testing</p>

<p>bilateral occiptial lobe lesion</p>

355
Q

<p>what is blindsight and what causes it?</p>

A

<p>individual can perform a task without conscious visual perception</p>

<p>visual cortex lesion</p>

356
Q

<p>What is Anton's Syndrome? What causes it?</p>

A

<p>Complete visual loss on confrontation testing + anosognosia</p>

<p>Bilateral occipital lobe lesion</p>

357
Q

<p>List some disorders involving the Inferior Occipitotemporal Cortex</p>

A

<ol> <li>Prosopagnosia</li> <li>Achromatopsia</li> <li>Micropsia, Macropsia</li> <li>Metamorphopsia</li> <li>Cerebral dipopia/polyopia</li></ol>

<p></p>

358
Q

<p>what is archromatopsia?</p>

A

<p>Difficulty with color perception</p>

<p>whole visual field involved = lesions in bilateral inferior occititotemporal cortex</p>

<p>one eye = contralateral cortical involvement</p>

359
Q

<p>what is micropsia and macropsia?</p>

A

<p>objects appear unusually small or big</p>

360
Q

<p>what is metamorphopsia?</p>

A

<p>objects have distorted shape or size</p>

361
Q

<p>what causes cerebral diplopsia/polyopia?</p>

A

<p>occipital lobe lesion</p>

362
Q

<p>List some syndromes of the Dorsolateral Parieto-Occipital Cortex</p>

A

<ol> <li>Simultanagnosia</li> <li>Optic ataxia</li> <li>ocular apraxia</li> <li>Baliant's syndrome</li></ol>

<p></p>

363
Q

<p>what is simultanagnosia?</p>

A

<p>impaired ability to percieve parts of a visual scene as a whole</p>

364
Q

<p>what is optic ataxia?</p>

A

<p>impaired ability to reach for or point to objects in space under visual guidance</p>

365
Q

<p>what is occular apraxia?</p>

A

<p>difficulty voluntarily directing one's gaze towards objects in peripheral vision</p>

366
Q

<p>what is Baliant's syndrome?</p>

A

<p>bilateral lesions of DL parieto-occipital cortex</p>

<p>presents with a clincial triad of the following symptoms:</p>

<ul> <li>simultanagnosia</li> <li>optic apraxia</li> <li>occular apraxia</li></ul>

<p></p>

367
Q

<p>Functions of the frontal lobe can fit into 3 categories, what are they?</p>

A

<ol> <li>restraint</li> <li>initiative</li> <li>order</li></ol>

<p></p>

368
Q

<p>list some restraint functions of the frontal lobe</p>

A

<ol> <li>judgement</li> <li>foresight</li> <li>perseverance</li> <li>delaying gratification</li> <li>inhibiting socially inappropriate responses</li> <li>self-governance</li> <li>concentration</li></ol>

<p></p>

369
Q

<p>List some initiative functions of the frontal lobe</p>

A

<ol> <li>curiosity</li> <li>spontaneity</li> <li>motivation</li> <li>drive</li> <li>creativity</li> <li>shifting cognitive set</li> <li>mental flexibility</li> <li>personality</li></ol>

<p></p>

370
Q

<p>list some Order functions of the frontal lobe</p>

A

<ol> <li>abstract reasoning</li> <li>working memory</li> <li>perspective taking</li> <li>planning</li> <li>insight</li> <li>organization</li> <li>sequencing</li> <li>temporal order</li></ol>

<p></p>

371
Q

<p>what is the difference in symptoms between a dorsolateral and ventromedial orbitofrontal lesion?</p>

A

<p>DL = apthetic, abulic</p>

<p>VM = impulsive, disinhibited, poor judgement</p>

<p></p>

372
Q

<p>what is the difference between a L and R hemisphere frontal lobe lesion?</p>

A

<p>left = associated with depression-like symptoms</p>

<p>right = more associated with behavioral disturbances like mania</p>

373
Q

<p>frontal lobe syndromes are also known as \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_</p>

A

<p>dysexecutive syndrome</p>

374
Q

<p>What types of symptoms are typically observed with an orbitofrontal lobe syndrome?</p>

A

<p>(disinhibited)</p>

<ol> <li>impulsive behavior (psuedopsychopathic)</li> <li>inappropriate jocular affect, euphoria</li> <li>emotional lability</li> <li>poor judgement and insight</li> <li>distractibility</li></ol>

<p></p>

375
Q

<p>what types of symptoms are typically observed with frontal convexity syndrome?</p>

A

<p>(apathetic)</p>

<ol> <li>apathy (pseudodepressive)</li> <li>indifference</li> <li>psychomotor retardation</li> <li>motor perseveration and impersistence</li> <li>stimulus-bound behavior</li> <li>motor programming deficits</li> <li>poor word list generation</li></ol>

<p></p>

376
Q

<p>What are some additional frontal lobe lesion symptoms?</p>

A

<ol> <li>disinhibition</li> <li>inappropriate jocularity (witzelsucht)</li> <li>limited insight</li> <li>utilization behavior/environmental dependence</li> <li>frontal release signs</li> <li>paratonia</li> <li>frontal gait</li></ol>

<p></p>

377
Q

<p>what is the symptom of disinhibition?</p>

A

<p>silly behavior, crass jokes, aggressive outbursts</p>

378
Q

<p>define inappropriate joculatiry (witzelsucht)</p>

A

<p>seemingly unconcerned about potentially serious matters</p>

379
Q

<p>what is utilization behavior/environmental dependence?</p>

A

<p>respond to whatever stimuli at hand, even when not appropriate</p>

<p>(also called new bed over syndrome)</p>

380
Q

<p>List some frontal release signs</p>

A

<ol> <li>palmar reflex</li> <li>grasp reflex</li> <li>sucking reflex</li></ol>

<p></p>

381
Q

<p>what is paratonia?</p>

A

<p>increase in tone, but in a manner in which patient appears to resist the movements of the examiner in almost a willful fashion</p>

382
Q

<p>define Frontal gait</p>

A

<p>shuffling, unsteady, magnetic gait</p>

383
Q

<p>what is being tested during the</p>

<p>light touch: localization test?</p>

A

<p>dorsal column</p>

<p>ability to detect and localize a light touch stimulus</p>

384
Q

<p>what is being tested during the pin prick test?</p>

A

<p>spinothalamic tract</p>

<p>ability to detect difference between sharp and dull sensation</p>

385
Q

<p>what is being tested during the hot:cold test?</p>

A

<p>spinothalamic tract</p>

<p>ability to detect between a hot and cold stimulus</p>

386
Q

<p>what is being tested during a vibration test?</p>

A

<p>dorsal column/medial lemniscus</p>

<p>ability to detect a vibration (when it starts and when it stops)</p>

387
Q

<p>what is being tested during the extinction test?</p>

A

<p>test for unilateral neglect</p>

<p>specifically tactile neglect</p>

388
Q

<p>what is being tested during the 2-point discrimination test?</p>

A

<p>dorsal column/medial lemnsicus tract</p>

<p>ability to accurately distinguish between 1 or 2 points of contact</p>

<p></p>

389
Q

<p>what is the normative data/distances for the 2-point discrimination test?</p>

A

<p>fingertips = 2-5 mm</p>

<p>palms = 8-12 mm</p>

<p>hand, extremities, trunk = 20-30 mm</p>

390
Q

<p>what is being tested in the proprioception test?</p>

A

<p>dorsal column/medial lemniscus tract</p>

<p>ability to detect position of limb when it is changed slightly (up/down)</p>

391
Q

<p>what is being tested during the stereognosistest?</p>

A

<p>dorsal column→ integrative ability of the parietal cortex</p>

<p>ability to accurately ID common objects based off of touch alone (eyes closed)</p>

392
Q

<p>what is being tested during the graphesthesia test?</p>

A

<p>dorsal column→ integration at parietal cortex</p>

<p>ability to accurately ID a letter/number that is drawn on your hand w/eyes closed</p>

393
Q

<p>what is being tested during the kinesthesia test?</p>

A

<p>dorsal column→ integration at parietal cortex→ motor cortex</p>

<p>ability to detect movement in space and then match it with the contralateral limb (eyes closed)</p>

394
Q

<p>how are all sensations tests graded?</p>

A

<p>5/5 = normal</p>

<p>1 - 4/5 = impaired</p>

<p>0/5 = absent</p>

395
Q

<p>what are the deep tendon reflexes for the UE/LE testing for?</p>

A

<p>presence or absense of an UMN/LMN lesion</p>

396
Q

<p>what nerve roots are responsible for the patellar tendon reflex?</p>

A

<p>femoral nerve (L2, 3, 4)</p>

397
Q

<p>what nerve roots are responsible for the achilles reflex?</p>

A

<p>tibial neve (S1, 2)</p>

398
Q

<p>what nerve roots are responsible for the biceps brachii tendon reflex?</p>

A

<p>musculocutaneous nerve ((C5, 6)</p>

399
Q

<p>what nerve roots are responsible for the brachioradialis tendon reflex?</p>

A

<p>radial nerve (C5, 6)</p>

400
Q

<p>what nerve roots are responsible for the triceps tendon reflex?</p>

A

<p>radial nerve (C6, 7)</p>

401
Q

<p>what are the grades/scores for reflex testing?</p>

A

<p>0-1+ = LMN</p>

<p>2+ = norma</p>

<p>3+ = Brisk</p>

<p>4+ and 5+ = UMN lesion</p>

402
Q

<p>what is the purpose of the Hoffman's sign?</p>

A

<p>it is a pathological reflex that indicates the presence or absence of an UMN/LMN</p>

<p>flexion of 1,2 phalanx = a positive sign</p>

<p></p>

403
Q

<p>what is the purpose and grading of the Babinski's sign?</p>

A

<p>tests for the presence/absence of an UMN/LMN</p>

<p>splaying of toes and ext of hallux is a positive sign</p>

404
Q

<p>what is the UE and LE synergy test for?</p>

A

<p>it tests the corticospinal tract and isolation of movement at a joint</p>

<p></p>

405
Q

<p>what is considered an abnormal result for an UE and LE synergy test?</p>

A

<p>movement in two or more joints in compensatory/synergistic pattern</p>

<p>this indicates an UMN lesion</p>

406
Q

<p>what does dysmetria (for UE and LE) test for?</p>

A

<p>cerebellar coordination/functioning</p>

407
Q

<p>what are abnormal results for dysmetria UE/LE?</p>

A

<p>hypometria = undershooting</p>

<p>hypermetria = overshooting, varying course of movement, disintegration of pattern</p>

408
Q

<p>what does dysdiadochokinesia test for?</p>

A

<p>cerebellar coordination/functioning</p>

409
Q

<p>what is included in a spasticity test?</p>

A

<ol> <li>shoulder FLX/EXT</li> <li>elbow FLX/EXT</li> <li>wrist FLX/EXT</li> <li>thumb flexors</li> <li>finger flexors</li> <li>hip FLX/EXT</li> <li>hip ABD/ADD</li> <li>knee FLX/EXT</li> <li>ankle DF/PF</li> <li>clonus</li></ol>

<p></p>

410
Q

<p>what does spasticity test for?</p>

A

<p>velocity dependent tone</p>

<p>presense of an UMN lesion</p>

411
Q

<p>how are spasticity tests measured?</p>

A

<p>Modified Ashworth Scale</p>

412
Q

<p>what results indicate the presence of clonus?</p>

A

<p>repeated bouncing of foot (plantarflexors)</p>

413
Q

<p>what results are you looking for when testing the papillary reflexes?</p>

A

<p>direct and consensual constriction</p>

<p>accommodation</p>

414
Q

<p>what is considered an abnormal result when testing the papillary reflex?</p>

A

<p>absense of constriction (direct/consensual)</p>

<p>absense of accommodation</p>

415
Q

<p>what is tested when performing the big H test?</p>

A

<p>EOMs</p>

<p>pursuit eye movements</p>

416
Q

<p>what are considered abnormal results from the big H test?</p>

A

<p>any asymmetry in movement</p>

<p>gaze palsies</p>

<p>2 or more of the following: nystagmus, strabysmus, saccades, and double vision</p>

417
Q

<p>what gaze palsies can be observed as an abnormal result from a big H test?</p>

A

<p>UMN = same direction limitation</p>

<p>LMN = opposite direction limitation or in one eye</p>

<p></p>

418
Q

<p>what are the grades that can be assignedduring a Weber and Rinne test?</p>

A

<p>normal</p>

<p>conductive loss</p>

<p>sensoryneuro loss</p>

419
Q

<p>what suggests conductive hearing loss during a Weber test?</p>

A

<p>positive is louder in affected ear</p>

420
Q

<p>what suggests neurosensory hearing loss during a Weber test?</p>

A

<p>positive weber =louder in unaffected ear</p>

421
Q

<p>what suggests conductive hearing loss during a Rinne test?</p>

A

<p>hear sound only in mastoid process</p>

<p>no sound heard when tuning fork is placed in front of auricle</p>

422
Q

<p>what suggests neurosensory hearing loss during a Rinne test</p>

A

<p>no sound hear at either the mastoid or in front of the ear</p>

423
Q

<p>when testing CN XI what indicates and UMN or LMN?</p>

A

<p>asymmetry in strength</p>

<p>UMN = trap is weak but SCM is spared</p>

<p>LMN = both are weak/absent</p>

424
Q

<p>define dysesthesia</p>

A

<p>unpleasant and abnormal sensation</p>

<p>can be evoked or spontaneous</p>

425
Q

<p>what are the 2 types of dyesthesia?</p>

A

<ol> <li>allodynia</li> <li>hyperalgesia</li></ol>

<p></p>

426
Q

<p>what is allodynia?</p>

A

<p>pain evoked by stimulus that is not usually noxious</p>

<p>(a cotton ball evoking pain)</p>

427
Q

<p>what is hyperalgesia?</p>

A

<p>excessive sensitivity to stimuli that are normally mildly painful</p>

428
Q

<p>T/F: when a part of the body is injured, special pain receptors convey the pain message to your brain</p>

A

<p>FALSE</p>

<p>incomplete concept</p>

<p>pain is a perception/experience</p>

<p>nociceptive fibers carry sensations that can be later interrpreted as pain</p>

429
Q

<p>what evidence is there that type C and A-delta fibers do not carry pain signals?</p>

A

<p>if they carried pain fibers then every time they were stimulated, the result should be the same pain.</p>

<p>Not the case, the same injury in the same person can cause different levels of pain depending on the context</p>

430
Q

<p>T/F: pain only occurs when you are injured</p>

A

<p>FALSE</p>

<p>injury or degeneration may be present in the absence of pain</p>

<p>significant pain may be present with no identifiable disease process or even after tissue healing</p>

431
Q

<p>pain is an emotional experience and can develop due to emotional overload. However it is important to not classify it as \_\_\_\_\_\_\_\_\_\_\_\_\_</p>

A

<p>a psychosomatic issue</p>

432
Q

<p>T/F: the timing and intensity of pain matches the timing and number of signals in nociceptors</p>

A

<p>FALSE</p>

<p>repeated signals from nociceptors to the dorsal horn of spinal cord can result in action potential windup leading to heightened sensitization</p>

433
Q

<p>what is action potential windup?</p>

A

<p>repeated stimulation of nociceptors to the dorsal horn of the spinal cord resulting in a progressive increase in action potentials</p>

434
Q

<p>what can action potential windup cause?</p>

A

<p>heightened sensitization</p>

<p>death of interneuron in dorsal horn⇒ decreased ability to modulate response</p>

<p>2nd order neuron receptors get replaced with receptors that increase danger messages to the brain</p>

435
Q

<p>T/F: Nerves have to connect a body part to your brain in pain</p>

A

<p>FALSE</p>

<p>phantom limb pain</p>

<p></p>

436
Q

<p>T/F: in chronic pain , the CNS becomes more sensitive to nociception</p>

A

<p>TRUE</p>

<p>due to:</p>

<ol> <li>action potential windup</li> <li>changes at the interneuron⇒ increased sensitization</li> <li>changes in descending modulation of pain</li></ol>

<p></p>

437
Q

<p>how does changes at the dorsal horn interneurons come about? How does this result in increased sensitization?</p>

A

<p>persistent input from C-fibers→ changes interneuron</p>

<p>→ changes in 2nd order neuron receptors→ sprouting and expansion of receptor fields→ increased sensitization</p>

438
Q

<p>T/F: the body tells the brain when it is in pain?</p>

A

<p>FALSE</p>

<p>the brain tells the body</p>

<p></p>

439
Q

<p>T/F: the brain sends messages down your spinal cord that can increase the nociception going up your spinal cord?</p>

A

<p>TRUE</p>

<p>changes in the CNS as a result of AP windup allow for increased info to be processed in the brain</p>

440
Q

<p>T/F: nerves adapt by increasing their resting level of excitment</p>

A

<p>TRUE</p>

<p>ion channels possess neuroplastic characteristics</p>

441
Q

<p>how often does ion expression change on a nerve?</p>

A

<p>continuously</p>

<p>half-life reported to be 48 hours</p>

442
Q

<p>T/F: Chronic pain mean that an injury hasn't healed properly</p>

A

<p>FALSE</p>

<p>injury and pain are not synonymous</p>

<p>not uncommon for a chronic pain pt to have no injury history</p>

443
Q

<p>T/F: receptors on nerves work by opening ion channels in the walls of the nerve</p>

A

<p>TRUE</p>

<p>ion channel expression constantly changes</p>

<p>ion channels are found on axons</p>

444
Q

<p>what is ion channel expression dependent on?</p>

A

<p>genetic coding</p>

<p>and</p>

<p>the brain's expression of the survival needs of the individual</p>

445
Q

<p>how is increased expression of certain ion channels impactful to chronic pain?</p>

A

<p>increased expression of certain ion channels may result in the development of sensitivity to the stimulus that opens that specific channel</p>

446
Q

<p>T/F: the brain decides when you will experience pain</p>

A

<p>TRUE</p>

<p>pain is a brain construct based on perception of threat</p>

447
Q

<p>T/F: worse injuries always result in worse pain</p>

A

<p>FALSE<br></br>stepping on a lego vs soldier not noticing getting shot</p>

448
Q

<p>T/F: when you are injured, the environment that you are in will not have an effect on the amount of pain you experience</p>

A

<p>FALSE</p>

<p>injuries in high stress environments are 7-8x more likely to result in persistent pain</p>

449
Q

<p>T/F: it is possible to have pain and not know about it</p>

A

<p>FALSE</p>

<p>the decision to produce pain is a conscious decision by the brain</p>

<p>this is why you aren't in pain while under anesthesia</p>

450
Q

<p>T/F: Nerves can adapt by making more ion channels</p>

A

<p>TRUE</p>

451
Q

<p>T/F: 2nd order nociceptor post-synaptic membrane potential is dependent on descending modulation</p>

A

<p>TRUE</p>

452
Q

<p>how should the placebo effect be viewed?</p>

A

<p>an endogenous mechanism to modulate the pain experience</p>

453
Q

<p>T/F: Nerves adapt by making ion channels stay open longer</p>

A

<p>TRUE</p>

<p>G-protein channels can remain open for minutes</p>

<p>in persistent pain, a greater concentration of G-protein channels may be seen in 2nd order neurons</p>

<p>can contribute to the windup effect</p>

454
Q

<p>T/F: when you are injured, chemicals in your tissues can make nerves more sensitive</p>

A

<p>TRUE</p>

<p>various chemicals can influence opening/closing of specific ion channels</p>

<p>Adrenaline and cortisol</p>

455
Q

<p>T/F: in chronic pain, chemicals associated with stress can directly activate nociception pathways</p>

A

<p>TRUE</p>

<p>the stress response</p>

456
Q

<p>using a the lion metaphor, describe the stress response if "the lion enters the room and follows you around for months/years"</p>

A

<p>if the stressors remain present for months, the stress response of increased adrenaline is then followed by cortisol changes in your body</p>

457
Q

<p>what is the IASP definition of pain?</p>

A

<p>pain is an unpleasant sensory and emotional experience which follows actual or potential tissue damage or is described in terms of such damage</p>

458
Q

<p>List 2 key things to keep in mind when defining what chronic pain is</p>

A

<ol> <li>it can be thought of as maladaptive neuroplasticity (increased sensitivity)</li> <li>associated with abnormal intracortical inhibitory mechanisms <ol> <li>smudging</li> </ol> </li></ol>

<p></p>

459
Q

<p>List the PNE Principles (summary)</p>

A

<ol> <li>pain is an output of the brain</li> <li>pain is not always an indicator of tissue damage</li> <li>the amount of pain you percieve does not = the amount of damage</li> <li>in chronic pain, the brain believes you are in danger and need protecting</li> <li>context of pain experience is vital</li></ol>

<p></p>

460
Q

<p>what is fibromyalgia?</p>

A

<p>chronic disorder</p>

<p>widespread pain, abnormal pain processing (pain amplification and impaired descending inhibition), sleep disturbances and fatigue</p>

461
Q

<p>what is chronic regional pain syndrome (CRPS)?</p>

A

<p>syndrome resulting in pain, vascular changes and atrophy</p>

<p>occurs in a regional distribution as opposed to a peripheral nerve or nerve root distribution</p>

<p>S/S worse in distal extremities</p>

462
Q

<p>when does CRPS usually occur?</p>

A

<p>secondary to trauma (surgery, fracture, crush injury, sprain)</p>

<p></p>

463
Q

<p>what is the primary complaint for CRPS?</p>

A

<p>severe, spontaneous pain, out of proportion to the injury</p>

464
Q

<p>what are the S/S of CRPS?</p>

A

<ol> <li>sensitivity to cold, pressure and touch</li> <li>early symptoms: <ol> <li>red/pale skin</li> <li>excessive sweating</li> <li>edema</li> <li>skin atrophy</li> </ol> </li> <li>later signs <ol> <li>skin becomes dry and cold and joints become stiff and swollen</li> </ol> </li> <li>motor signs (paresis, spasms, and tremor)</li></ol>

<p></p>

465
Q

<p>what is the primary precipitating factor for CRPS?</p>

A

<p>disuse</p>

DPT Semester 2 (6 decks)

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