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My sem 3 > case 7 > Flashcards

case 7 Flashcards

1
Q

MPTP

A

produces parkinsonism by destroying nigral cells, accidental exposure, neurotoxic cause crosses BBB destroys nigral cells. Manganese oxide can also cause PD

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2
Q

cognitive labelling theory

A

: Physiological arousal is necessary for
emotional experience but the nature of the arousal is
immaterial: its how we label it that matters

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3
Q

5 components of an emotional system

A

expression changes. physiological arousal. behaviour. subjective affect. cognitive appraisal.

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4
Q

james lange theory of emotions

A

Emotionally significant events lead to physiological changes and the
experience of emotion is a CONSEQUENCE of these bodily responses

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5
Q

cannon bard theory of emotions

A

Emotionally significant events INDEPENDENTLY cause emotional

experience and physiological responses.

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6
Q

fear

A

lesions in amygdala down abolish it.

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7
Q

striatum

A

caudate and putamen

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8
Q

Direct basal ganglia pathway

A

glutamate signals to striatum, inhibitory signal to GPi and SNpr. So no longer able to inhibit thalamus. thalamus sends ok message to cortex to allow movement. SNpc sends dopamine to D1 causing it to be more active.

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9
Q

indirect basal ganglia pathway

A

frontal lobes send excitatory signal to striatum, striatum inhibitory to GPe. GPe no longer inhibits STN. STN active excitatory signal to GPi. GPI more inhibitory so thalamus more inhibited so doesnt send message to motor cortex, dec movement. DA binds D2 inhibitory of this pathway so more excitation of movement.

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10
Q

acetylcholine

A

major efferent NT of PNS. AcoA and choline with choline acetyltransferase. Hydrolysed by acetylcholinesterase into acetate and choline. muscarinic receptors most in brain.

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11
Q

glutamate

A

excitatory neuron in CNS. elevated conc in neural injury is toxic to neurons. Doesnt cros BBB so synth in neurons from glucose or glutamine. Glutamine released glial cells, glutaminase turns it. back to glutamine via glutamine synthetase. Ionotropic (NMDA AMPA) allow passage of NA K Ca. when hyperpolarised Mg blocks pore. requires glycine.

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12
Q

GABA and glycine

A

inhibitory. GABA formed from glutamate by glutamic acid decarboxylase GAD. converted to succinate by GABA transaminase. GABAa and GABAc ionotropic. GABAb metabotropic. GABAb inhibit Ca channels activate K. glycine is abundant in the spinal cord grey matter of ventral horn.

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13
Q

substantia nigra

A

latin for black substance due high levels of neuromelanin. nigrostriatal pathway arises from SNoc and projects to caudate and putamen. primary input to basal ganglia. dysfunctions or degeneration of cells cause parkinsons.

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14
Q

ventral tegmental area

A

mesolimbic pathway - VTA to limbic structures, reward. Mesocortical-VTA to PFC. working memory and attention.

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15
Q

input into basal ganglia

A

corticostriatal pathways largest source, through internal capsule to striatum. visual and auditory dont go here. topographically mapped. medium spiny neurons. spines allow to integrate inputs from variety of cortical thalamic and brainstem structures. axons synapse on GP and SNpr. Sensory and motor go to putamen, PFC caudate.

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16
Q

output from the basal ganglia

A

medium spiny neurons go to GP and SNpr. GABA then to GPi SNpr. direct. or indirect pathway.

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17
Q

interneurons

A

can be inhibitory or ecitatory.

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18
Q

D1 D2

A

D1 inc dynorphin which stimulates direct pathway. D2 dec enkephalin which inhibits indirect pathway.

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19
Q

ansa lenticularis

A

course from GPi to thalamus, looping course ventrally under internal capsule.

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20
Q

lenticular fasciculus

A

straight through internal capsule pass STN before turning to enter thalamus. join with ansa lenticularis to form thalamic fasciculus.

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21
Q

lobes of cerebellum

A

anterior posterior and flocculonodular (functions with vestibular system) each fold is called a folium.

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22
Q

cerebrocerebellum

A

regulates highly skilled movements. eye movements. speech, hand eye coordination. projects to dentate nucleus.

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23
Q

vestibulocerebellum

A

comprises flocculus and nodulus. posture and equilibrium. projects to lateral vestibular nucleus.

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24
Q

spinocerebellum

A

medial part. input directly from SC. movements distal proximal and eye movements. projects to fastigial and interposed nuclei.

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25
Q

superior cerebellar peduncle

A

output from cerebellum. post lobe to midbrain.

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26
Q

middle and inf cerebellar peduncle

A

inputs. from medulla to ant lobe sensory info about posit of body. middle from pontine nuclei desired position of body. from ipsilateral side of body.

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27
Q

dentate nucleus

A

all outputs originate from the deep nuclei so a lesion to the nuclei is like a lesion to the entire cerebellum. a lesion will effect the ipsilateral side of the body unlike the cortex. recieves input from the lateral cerebellar hemispheres and from cerebellar afferents from the corteex, projects to the red nucleus and VL thalamic nucleus.

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28
Q

fastigial nucleus

A

most medially, inout from the vermis and afferents carrying vestibular, auditory and visual info. projects to the vestibular nuclei and reticular formation

29
Q

interposed nucleus-emboliform and globose.

A

lateral, recieve input from intermediate zone and afferents from spinal somatosensory auditory and visual. project to red nucleus.

30
Q

vestibular nucleus

A

not part of cerebellum but recieve input from floccunodular lobe and vestibular labrinth, start of vestibulospinal tract.

31
Q

3 cell layers and 5 cell types

A

outer molecular layer-consists of aons of various cerebellar neurons. Middle layer-single layer of large neurons Purkinje cells. Granular layer-densly populated with granule cells.
Cell types purkinje granule basket stellate and golgi.

32
Q

mossy fibres and climbing fibres

A

afferent fibres that provide input into the cerebellar cortex. mossy fibres axon terminal ends in a large bulbous swelling, enter granular cell layer and synapse on dendrites. Each fibre innervates 600 granule cells, which recieve inout from 4 fibres. send axons up the molecular layer and run parallel-parallel fibres. synapse on purkinje. climbing fibres go straight to the purkinje dendrites and climb up them. One to one. come from inferior olivary nucleus through inf peduncle. then go to deep nuclei.

33
Q

stellate basket and golgi cells

A

inhibitory neurons, help limit surround inhibition so focus cerebral cortex output.

34
Q

archicerebellum

A

flocculonodular lobe and fastigal nucleus. primarily concerned with balence. vestibulocerebellum

35
Q

paleocerebellum

A

vermis, paravermis and globose and emboliform nuclei. concerned with maintenacne of muscle tone and posture. spinocerebellum.

36
Q

neocerebellum

A

ant and post cerebellar hemispheres and dentate nucleus. concerned muscle coordination. cerebrocerebellum

37
Q

dorsal spinocerebellar tract

A

afferent info about lower extremity limb movements. primary sensory neurons carrying propriceptive touch and pressure enter via dorsal roots and ascend in gracile fasciculus, some form synapses in nucleus dorsalis of clark, ascend ipsilaterally in spinocerebellar tract, mossy fibres to inf cerebellar peduncle.

38
Q

cuneocerebellar tract

A

afferent info from upper extremity limbs. enter cuneate fasciculus synapse external cuneate nucleus in medulla, ascend in inf cerebellar peduncle.

39
Q

ventral spinocerebella tracts

A

info about activity of spinal cord interneurons from lower extremity. from spinal border cells. superior cerebellar peduncle.

40
Q

rostral spinocerebellar tract

A

convey info about activity of spinal cord interneurons of upper extremity. through inf and sup cerebellar peduncle.

41
Q

Parkinsons disease

A

characterised by resting tremor, rigidity, bradykineasia and gait impairment. degeneration of fopaminergic neurons in substantia nigra pars compacta so less L DOPA. 2nd most common neurodegenerative disease after dementia. 1.5/1000. age onset 60. reduced risk with smoking and caffeine. symptoms show once DA has fallen to 20-40%. Rigidity and tremor caused by other neurochem disturbances as well as DA.

42
Q

causes

A

mutation in the LRRK2 gene 1% of disease most common mutation, encodes protein dardarin. Parkin gene mutation likely in early onset, lack of lewy bodies. SNCA gene cause problems in a-synuclein (protein that helps nerve cells communicate) cause Lewy bodies. GBA five fold risk.

43
Q

Lewy bodies/neurites

A

misfolding and aggregation of proteins. either by impaired clearence or inc formation (mutations in a-synuclein) usually cleared by ubiquitin proteasome system or autophagy/lysosome pathway.

44
Q

pathophysiology of PD

A

loss of nigrostriatal DA neurons in SNpc. normally compacta input to striatum causes ecitation of direct and inhibition of indirect. so when compacta cells destroyed inhibitory to BG very high so thalamic activation of UMN in motor cortex less likely to occur. dec dynorphin and inc in enkephalin.

45
Q

normal compensations to loss of DA

A

boost level of activity or inc sensitivity in striatum. account 75% loss. Ach is also affected by loss DA.

46
Q

bradykinesia and hypokinesia

A

reduced DA means more inhibitory input to basal ganglia so difficult to initiate movements.

47
Q

rigidity

A

muscle spindles inc muscle tone as inc M2 after arrest voluntary movement. also may be effected by reticulospinal tract as innervated pontine nuclei which is connected to basal ganglia, so Ia inhibition increases so more a muscle contraction.

48
Q

resting tremor

A

involves basal ganglia and cerebello thalamo cortical circuit. dec DA causes activity in striato pallidal circuit which triggers tremor in cerebello thalamo cortical circuit. only at rest when BG not involved in voluntary movement.

49
Q

intention tremor

A

cerebellar tremor, triggered by movement towards a target. damage to cerebellum. not usually seen in PD.

50
Q

other signs and symptoms

A

resting and pill rolling tremor. cogwheel rigidity. posture stooped balance is difficult. less facial expresions. swallowing difficulties. speak softly and stutter. micrographia. gait. insomnia. urinary hesitancy. constipation. loss of smell. dementia.

51
Q

diagnosis

A

must have bradykinesia.finger tapping test. fast foot tapping. observation of handwriting. absent arm swing when walking.

52
Q

PET scan

A

3D image of functional processes. detects gamma rays. radiotracer is tagged to a natural chamical. 18F-flurodopa, tagged to DA. dec in PD in SN. detects the energy emitted by positrons. gamma waves released.

53
Q

SPECT scan

A

gamma camera takes 2D image at different angles and a computer makes 3D. cheaper than PET lower resolution.

54
Q

co beneldopa

A

Levadopa-precurser DA as DA cant cross BBB. used alongside peripheral DA decarboxylase inhibitor. SE:dyskinesia at peak therapeutic effect. rapid fluctuations in clinical state, on off phenomenon, fluctuating plasma concs, as disease advances the ability of neurons to store DA is lost, so more LDOPA needed, sustained release may help fluctuations. nasea hypotension delusions.
Benserazide used alongside to prevent decarboxyation of LDOPA in periphery. cant cross BBB. DOPA decarboxylase inhibitor. allowing DA to build up solely in brain.

55
Q

selegiline

A

MAO B inhibitor. irreversible. blocking metabolism enhancing DA activity in SNpc. Its metabolised to amphetamine which can cause excitement.

56
Q

NICE treatment options

A

Levadopa - dopamine agonist - MOAB COMT inhibitor - b blocker - amantadine - anticholinergics. apomorphine.

57
Q

other treatment

A

physiotherapy to help with gait, balence. occupational therapy. speech and language therapy help swallow.

58
Q

limbic system

A

involved in memory behaviour emotion and olfaction. forms a border around corpus callosum and brain stem. consiste of the parahippocampal gyrus, cingulate gyrus and subcallosal gyrus.

59
Q

hippocampal formation

A

hippocampus, dentate gyrus and parahippocampal gyrus. memory learning and spatial navigation. lies along floor of inf horn of lat ventricle. dentate gyrus extends from hippocampus to parahippocampal gyrus.

60
Q

amygdaloid body

A

involved in formation and storgae of memories. fear conditioning and sense of smell. recieves input from association cortices, cingulate gyrus, olfactory bulb and BS. located ant end of caudate nucleus in temporal lobe.

61
Q

fornix

A

connexts post part of hippocampus with mamillary bodies of hypothalamus. divided into crus body and commissure and ant columns.

62
Q

stria terminalis

A

connects amygdaloid body with ant hypothalamus and septal nuclei.

63
Q

mamillothalamic tract

A

connects mamillary bodies of hypothalamus with ant nuclei of thalamus.

64
Q

olfactory system

A

linked to taste, loss of smell is termed anosmia. SNC and nasal septum covered with olfactory mucosa. olfactory neurons are bipolar, ciliated receptors. Pathway: enter skull through cribiform plate. terminate in olfactory bulb by synapsing with mitral and tufted cells. enter olfactory tract. divide into medial and lateral striae. most in lateral, go to primary olfactory cortex-uncus and amygdaloid body. medial go to anterior commissure to contralateral olfactory bulb.

65
Q

diencephalon

A

thalamus, sub, epi and hypothalamus.

66
Q

functions of the hypothalamus

A

endocrine, temperature, homeostasis, water balence

67
Q

which part of the basal ganglia comes from telencephalon

A

caudate putamen GPi e

68
Q

which part comes from diencephalon

A

STN

69
Q

which part comes from mesencephalon

A

Substancia nigra

My sem 3 (16 decks)

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