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1
Q

Snellen

A

Number on each line is distance a normal person can read those size letters from.
-reporting
1st number- distance they read it from (6m)
2nd number- smallest line they read correctly
-so 6/6 vision is normal
6/5 is better than normal.

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2
Q

LMN

A

Cell bodies collect to form discrete motor nuclei of CNs in brainstem or ventral horn SC.
Axons to skeletal muscle. Leave as motor divisions of CNs or spinal segmental Ns.
Alpha or gamma types. Alpha usually constant inhibition from UMNs, especially EP (so UMN lesion= hyper). This is lifted to allow move.

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3
Q

Motor unit

A

An alpha MN and the muscle fibres it inenervates.
Get larger with age.
Fibres not reinnervated atrophy and become CT= stiff.
Lots in EO muscles= precision, less in gastrocnemius.
-classification-
S- slow, fatigue resistant, small force, oxidative metabolism, well vascularised, red.
FR- fast contracting, fatigue resistant, low force, oxidative but some glycoltyic.
FF- fast, fast fatigue, high force, glycolytic, low vascularisation, pale.
Recruit in order.

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4
Q

MU frequency of activation controls force

A

Tetany- impulses so close together= smooth contraction. Fatigue and cramp fast as compress BV.
Unfused- tremor. Asynchronous MU activation. Maintains BS as contraction AND relaxation phase.

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5
Q

Control muscle force

A

Frequency of MU activation

Number and type of MU activated

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6
Q

Spinal reflex proprioceptors

A

Muscle spindle- muscle stretch
Tendon organ- contractile tension
Joint Rs- joint movement
Skin- skin stretch

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7
Q

Large fibre sensory neuropathy

A

Large sensory afferents die.
Often post viral or AI.
Lose spindle feedback so need visual control to do a movement.
Lose reflexes so cant maintain posture.

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8
Q

Hughlings jackson neuro lesions

A

Negative- loss of function or capacity

Postive- emergence of a feature.

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9
Q

UMN (pyramidal and extra)

A

Celll body in cerebral (motor areas- motor, pre, suppmentary, somatosensory) cortex or brainstem.
Remain in CNS.
MOST ARE INHIBITORY except a few CST.
Hypertonia (spastic paralysis), hyperreflexia.
Extra pyramidal lesion- uncontrolled movement, aberrant reflexes.
Pyramidal tracts monosynaptic contact LMNs.
Extrapyramidal indirect contact with rest of MN pools.

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10
Q

Corticobulbar are last to mature.

A

Complete by 17-18yo.

Myelination and function.

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11
Q

Motor cortex

A 
Not involved in planning- that is PMA and SMA,
Outputs to pyramidal tracts.
Inputs from PMA, SMA, SI.
Codes for force of specific muscles. 
Active 100ms before movement.
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12
Q

Pre motor cortex

A

Active 800ms before move.

Codes motor plans nd body set.

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13
Q

Supplementary motor area

A

Active 800ms before.

Codes motor plan, especially complex movements.

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14
Q

UMN lesions

Damage motor tracts and SC.

A

Signs often widespread eg mono/ hemi paresis.
No wasting or fasciculation.
Clasp knife- resistance then sudden.
Hypertonia, hyperreflexia, clonus.
Extensor plantar response- great toe extension, other toes flare.
Weakness
Causes- stroke (hemiparetic gait), SC injury.
-pyramidal- UMN signs, impair volition of fine movement.
-extra- impair way carry out movement eg gait.

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15
Q

Dorsal root lesion

A

All modalities lost
Possible hyporeflexia
Power and tone normal

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16
Q

SN complete lesion eg slip disc, vertebral fracture, stab

A

Sensory effects- ipsilateral, in dermatome.
Motor- myotome weaknes not complete loss as other SNs supply.
LMN signs.

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17
Q

Entire cord level destroyed

A

Loss LMN bodies to segment root and secondary sensory.

LMN signs at that level.

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18
Q

Dorsal horn lesion eg stab

A

Motor- LMNs spared as ventral horn. Lateral CST spared so motor ok.
BUT proprioception affected as dorsal column damage.
Sensory- Ipsilateral loss below the lesion of DCML modalities.
At the level of lesion get dermatome loss all modalities as DH destroyed.

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19
Q

Central canal lesion eg tumour growing centrally

SYRINGOMYELIA

A

Motor- ok as not affect DH.
Some weakness and UMN signs in trunk.
Sensory- secondary neurones decussate through ventral white commisure. Loss STT modalities (pain, temo, crude touch) bilaterally at level of lesion. Classically in cervical region- CAPE loss.

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20
Q

Bladder control lesions

A

Destroy S2-4= LMN effects in bladder- hypotonic, no sensory innervation. Require catheter.
In UMN lesion SC injury= back to reflex control as lost decending innervation.

21
Q

LMN lesions

Damage to cranial or spinal motor nuclei, or peripheral Ns.

A

Signs map distribution of the affected N.
Weakness, wasting, hypotonia (flacid paralysis), hyporeflexia, fasciculation (eg MND).
Causes of lesions- trauma, peripheral neuropathy, MND.
LMN lesions are in lower CNS or PNS.

22
Q

Spinal shock after descending tract severe damage

A

Weeks to months.
Ventral root intact BUT LMN signs eg flacid paralysis, areflexia.
Areflexia Possibly due to loss motor influences descending from RF. As these fibres degenerate the intact reflex connections become dominant= UMN signs.

Eventually spastic and hyperreflexive.

23
Q

Motor planning

A

Loop- cerebral cortex, cerebellum, basal ganglia, thalamus.

24
Q

Error correction

A

Spinal reflex
Brainstem and cerebellum
Cortical concious

25
Q

Cerebellar function

A

Coordinates motor output (voluntary, posture, gait)
Vestibulocerebellum (flocculonodular)- balance and ocular reflexes.
Spinocerebellum (paleo)- error correction, gait.
Cerebrocerebellum (neo)- planning and motor learning. Postural tone, modulation motor skills.

26
Q

Cerebellar dysfunction

A

Dysmetria, dysdiadochokinesia.
Ataxia
Nystagmus- maximal on gaze towards cerebellar lesion. (Vs away from vestibular).
Intention tremor
Speech (scanning dysarthria)- slurred or stoccato
Hypotonia
Also- cant learn new movement and balance problems.

27
Q

Cerebellar dysfunction causes

PASTIRES

A 
Posterior fossa tumour
Alcohol
MS
Trauma
Rare
Inhertied eg friedrichs ataxia
Epilepsy meds eg carbamazepine, phenytoin
Stroke
28
Q

Basal ganglia

Movement planning- regulate amplitude and velocity of planned movement, particularly regarding proprioceptive info.

A 
Caudate nucleus
Putamen
Globus pallidus 
SN
Subthalamic nucleus 
(Caudate+ putamen= neostriatum)
(Putamen + globus= lenticular nucleus)
-input from motor cortex, output to thalamus 
-dysfunction= hyperkinetic eg huntingtons, hypokinetic eg PD. Abnormal coordination and muscle sequencing.
29
Q

PD

A

Progressive degeneration of dopaminergic neurones of SN (nigrostriatal path). So less inhibitory output from striatum so NOT remove inhibition to thalamus. So less excitatory feedback to cortex and less excitation to brainstem and SC.
S+S-
7hz resting tremor reduced by moving. Pill rolling.
Increased tone- lead pipe or cog wheel (tremor+hypertonia, excentuated by distraction while moving arm) rigidity.
Bradykinesia
Hypertonia
Postural instability
-Gait- shuffling, festinating, reduced arm swing, pedistal turning, tremor, flexed.
-tx- L dopa precursor. DBS globus to prevent its inhibition.

30
Q

Huntingtons chorea

A

Neurodegeneration involves striatum.
Degeneration inhibitory neurones so excess activation directly.
Involuntary movement.
No cure.
Px 3rd/4th decade. Die in 5yr from other cause.

31
Q

Basal ganglia and PD

A

Direct path- dopamine= increase movement. Dopamine from SN to D1 Rs.
Indirect path- dopamine also= increase movement. SN to D2 Rs= less inhibition.

32
Q

Syringomyelia

A

Fluid filled cavity (syrinx/cyst) in SC. Expands and elongates= damage and compress Ns. Can include hydromyelia (dilation central canal by CSF).
Causes- idiopathic, tumour, SC injury, CSF blockage (arachnoiditis), haemorrhage, meningitis, trauma.
Highly variable px, slowly progressing.
Sensory loss in a “cape” distribution (over the tops of the shoulders); loss of pain and temperature sensation with preserved touch and position sense.
Cervical and occipital pain, extremity pain.
Hand and arm weakness and atrophy.
Spasticity.
In primary spinal syringomyelia, symptoms may appear months or even years after the initial injury, starting with pain, weakness and sensory impairment often originating at the site of trauma.

33
Q

Peripheral neuropathy glove and stocking

A

Symmetrical peripheral N lesions.
Loss all sensory modalities glove and stocking.
Demyelinating eg guillain barre
Axonal degeneration eg systemic, metabolic, toxic, nutritional disorders.
-possible causes-
Diabetes mellitus
Shingles (post herpetic neuralgia)
Vitamin deficiency, particularly B12 and folate
Alcohol
Autoimmune diseases, including lupus, rheumatoid arthritis or Guillain-Barre syndrome
AIDS, whether from the disease or its treatment, syphilis, and kidney failure
Inherited eg amyloid or charcot marie tooth.

34
Q

Oedema causes

A 
HF
Constrictive pericarditis
Venous stasis
Lymphoedmea
Nephrotic syndrome
Liver disease
Drugs
Immobility
35
Q

Drugs causing dyspnoea

A

BB
CCB
NSAIDs

36
Q

Drugs causing dizziness

A

Nitrates
ACEi
Alpha blockers
AngII R blockers

37
Q

Drugs causing angina

A

Thyroxine
Drug induced anaemia eg cimetidine
NSAIDs

38
Q

Drugs causing oedema

A

Steroids
NSAIDs
CCB

39
Q

Drugs causing palpitation

A 
Thyroxine 
Beta 2 agonist
Digoxin
Diuretic hypoK
TCA
40
Q

Drugs causing ataxia

A

Phenytoin
Carbamezepine
Lithium

41
Q

Drugs causing seizure

A

TCA
Phenothiazine
Clozapine

42
Q

Drugs causing myopathy

A

Statins

Steroids

43
Q

Drugs causing headache

A

GTN

Sildenafil

44
Q

Drugs causing peripheral neuropathy

A

Chemo
Metronidazole
Amiodarone
Antiretrovirals

45
Q

Drugs causing tremor

A

Beta agonist
Lithium
Valproate

46
Q

Causes of muscle weakness

A
  • LMN- peripheral neuropathies, mononeurpathies, radiculopathies, anterior horn damage eg poliomyelitis and MND.
  • UMN patterned weakness (lef ext, arm flex)- stroke, SC pathology, MS, brain tumour.
  • myopathies (proximal weakness)- muscular dystrophies, inflammation, CS, alcohol.
47
Q

Reflex N roots

A
  • bicep and brachioradalis- C5/6
  • triceps- C7
  • knee- L3/4
  • ankle- S1
48
Q

Sensory ataxia rhombergs postive

A

Vit B12 deficiency
Tabes dorsalis
Peripheral neuropathies
Firedrichs

causes of signs (13 decks)

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