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causes of signs > Peripheral N Signs > Flashcards

Peripheral N Signs Flashcards

1
Q

MRC power scale

A

0-no muscle movement
1-flicker
2-movement with gravity eliminated
3-movement against gravity but no against resistance
4- movement against resistance but not normal
5- normal power

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2
Q

Rhombergs

A

Cerebellar disease- sway with eyes open

Proprioception loss- sway with eyes closed.

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3
Q

Gait

A

Observe posture, arm swing, step size and frequency, circumduction, ataxia.
PD- shuffling, flexed, no arm swing, lean forward, difficulty stopping and changing direction.
Cerebellar ataxia- wide base, sway with eyes open, hold onto things.
Hemiparesis- arm flexed and adducted, leg extended and cirucmducted when brought around (cant flex knee).
Arthritis antalgic- limp due to pain
Foot drop- lateral popliteal palsy, high stepping.
Peripheral neuropathy- loss joint position sense, high stepping or stomping as unaware of foot position, very careful.

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4
Q

Pronator drift

A

UMN lesion

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5
Q

Clasp knife

A

UMN lesion

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6
Q

Lead pipe or cog wheel rigidity

A

Extra pyramidal lesion

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7
Q

Finger to nose

A

Stretch system- reposition backwards, forwards and laterally.
Proprioception deficit- bring outstretched finger to nose with eyes closed.
Cerebellar disease- intention tremor and past pointing.

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8
Q

Clonus

A

UMN lesionif over 5 beats of plantar felxion.

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9
Q

Cerebellar ataxia gait

A

Unsteady, broad base, worse with tandem walking, may have associated signs (nystagmus, dysarthria, limb signs).
Causes- MS, vascular cerebellar disease, chronic alcohol, paraneoplastic syndrome.

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10
Q

Hemiparetic gait

A

Legs stiff and swing out, flexion or UL and extension of LL.
causes- cortical or internal capsule strokes, cerebral hemisphere tumour or trauma.

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11
Q

Spastic gait

A

Legs slow and stiff, hips adducted and feet plantarflexed. (Scissors)
Causes- SC compression, cerebral palsy, MS, MND, SC degeneration.

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12
Q

Parkinsonian gait

A

Flexed, loss arm swing, multiple steps to turn, difficulty initiating, festinating gait.
Causes- IDP, drug induced eg antipsychotics, vascular pseudoPD, infection, wilsons.

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13
Q

Sensory ataxia

A

Broad base, unsteady, stamping, impaired proprioception, rhombergs positive.
Causes- posterior SC lesions, peripheral neuropathy.

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14
Q

High stepping gait

A

Cant dorsiflex, slapping foot.

Causes- comm fibular N palsy eg fibular head fracture. Hereditary eg charcot marie. Anterior horn disease eg polio.

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15
Q

Myopathic gait

A

Weight alternative sites, opposite trunk tilting. Weak proximal muscles of lower limb girdle.
Causes- MDs, endocrine or metabolic myopathies, polymyositis or dermatomyositis.

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16
Q

Brown sequard

A

SC hemisection=
-ipsialteral UMN weakness below lesion due to CST lesion.
-ipsilateral loss proprioception and vibration due to DCML.
-contralateral pain and temperature loss due to SST lesion (already decussated).
Causes eg butler, stab, tumour, disc herniation.
Diagnosis- MRI.

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17
Q

Guillain barre syndrome

A

Acute inflammatory demyelination polyneuropathy.
Signs- symmetrical ascending muscle weakness a few weeks after infection eg campylobacter, CMV, mycoplasma, zoster, EBV, vaccines.
Abs attack nerves.
Autonomic dysfunction- sweaty, tachyc, BP change, arrhythmia.
Increase protein in CSF.

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18
Q

Amyloidosis

A

Abnormal EC protein deposits in fibrils, resistant to degradation.
Eg AD, T2DM.
Systemic forms affect most systems.
Biopsy postive congo red stain.

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19
Q

Parasthesia

A 
Low Ca, high CO2
Arterial emboli, DVT
Lyme disease, rabies
ACEi
Thalam IC or parietal lesion
CTS, sciatica
Peripheral neuropathy eg DM, CKD.
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20
Q

Tremor

A
  • resting- PD
  • postural- worse if arms outstretched. Hyperthyroid, alcohol. Brain damage from wilsons, syphillis.
  • intention- worse when move. Cerebellar disease.
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21
Q

Brain BS modulation

A
  • myogenic- low BP=vasoldilation to maintain flow. Fails under 50mmHg
  • metabolic- high pCO2, K, adenosine, or low pO2= vasodilation
  • cushings reflex- RICP=reduced cerebral BF= SNS peripheral vasoconstriction= increase AP. POSITVE FEEDBACK.
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22
Q

ASCENDING concious tracts (contralateral)

A

-DCML:
2TPV- 2 point discrimination, fine touch, concious proprioception, vibration.
Primary body in DRG, secondary in gracile or cuneate nucleus, tertiary in thalamus.
Decussation in medulla.
Termination sensory cortex.
-STT:
Lateral- pain, temperature
Anterior- crude touch
Primary body in DRG, secondary in DH, tertiary in thalamus.
Decussation SC
Termination sensory cortex

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23
Q

ASCENDING CEREBELLAR unconscious tracts (ipsilateral)

A 
-anterior and posterior spinocerebellar:
Unconcious proprioception lower limb. 
Primary body DRG, secondary in spinal GM (posterior clarke nucleus, anterior spinal border), NO tertiary body. 
Posterior NO decussation.
Anterior decussates SC and brainstem.
Termination in cerebellum. 
-cuneocerebellar- 
Unconscious proprioception upper limb. 
Primary body DRG, secondary accessory cuneate nucleus.
Termination cerebellum.
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24
Q

ASCENDING tract lesions

A 
-DCML-
SC lesion= ipsilateral sensory loss as not CO until medulla. 
VitB12 deifciency 
Neurosyphillis tabes dorsalis
-STTs-
Contralateral as CO immediately. 
Brown sequard hemisection- ipsilateral loss fine touch, vibration, and proprioception. Contralateral loss pain and temperature. 
-SC-
Ipsilateral loss muscle coordination. 
Unlikely isolated damage.
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25
Q

DESCENDING pyramidal tracts

A 
-lateral CST 85%- 
Voluntary movement 
Origin pre motor and motor cortex, PCG. 
Decussation medulla. 
Termination contralateral SC. 
-ventral CST 15%-
As above but decussates SC. 
-corticobulbar-
Voluntary movement 
Origin pre motor and motor cortex, and PCG.
Decussation brainstem
Termination contralateral motor CN nuclei.
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26
Q

DESCENDING extra pyramidal tracts

A 
-TS-
Head movement towards visual or auditory stimulus. 
Origin tectum. 
Decussation brainstem. 
Termination C+upper T SC. 
-rubroS-
Flexor and facial tone
Origin red nucleus
Decussation brainstem
Termination upper C SC
-reticuloS- 
Automatic movement (posture and rhythmic)
Origin reticular formation
Decussation ? Part in brainstem
Termination SC
-VS-
Balance and posture
Origin vestibular nucleus
NO decussation
Termination SC
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27
Q

DESCENDING tract lesions

A

-CST-
Internal capsule CVA. Unilateral lesion= contralateral symptoms.
Typically UMN signs
-CBT-
Most are bilateral so unilateral lesion usually= mild muscle weakness only. EXCEPT- hypoglossal N UMN lesion spastic contralateral paralysis of genioglossus causing contralateral tongue deviation + facial N UMN lesion spastic paralysis contralateral lower quadrant face muscles.
-extra pyramidal-
Degenerative disease eg encephalitis or tumour. Dyskinesia or involuntary movement.

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28
Q

Pain

Lateral STT

A

Slow dull C fibres (70%)- respond to mechanical, chemical, thermal. Small diameter, unmyelinated.
Fast sharp Ad fibres- mechanothermal only.
Ligand gated TRPV1 channel- H+, heat and endocanniboids activate mainly Ca flow. Plus inflammatory mediator= pain.
-Gate control- dorsal horn lamina 2 substantia gelatinosa inhibits nociceptor transfer to thalamus. Nociceptor input and descending inhibitory control from raphe, PAG, brainstem. Also mechano Ab Rs.
-peripheral sensitisation- tissue damage= immune cells= histamine, 5HT, bradykinin, substance P, PGs. Directly cause pain or potentiate.
-central sensitisation- tissue injury= persistent glutamate release and high NMDA R activation= hyperexcitable neurones= hyperalgesia (lower threshold).
Wind up= receptive field expansion and allodynia (non noxious stim).

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29
Q

Middle cerebral A

A

Most common ste of stroke.

Supplies frontal, parietal and occipital.

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30
Q

ICA branches in circle of willis

A

Ophthalmic
Posterior communicating (aneurysm= CN III palsy)
Anterior choroidal

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31
Q

Cerebral infarct causes

A 
Large vessel atheroma or emboli. 
Cardiac emboli.
Small vessel disease or lacunae. 
Arteritis.
Blood disorder.
Cryptogenic.
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32
Q

Intra cerebral haemorrhage causes

A 
HTN microaneurysm 
AVM or aneurysm
Amyloid angiopathy
Anitcoagulation
Thrombolytic
Thrombocytopenia 
Cocaine, amphetamine
Tumour
VT
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33
Q

SC BS

A

Posterior- paired posterior spinal As
Anterior- anterior spinal A- motor area. Occlusion most common.
Also 21 pairs segmental As
Artery of Adamakiewics

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34
Q

Anterior spinal A occlusion causes

A 
Aortic disease eg aneurysm, trauma, dissection, atherosclerosis, surgery. 
Vasculitis 
SCD
Hypotension
TIA
Disc herniation
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35
Q

Spinal shock

A

Initial LMN signs, then progress to UMN.

Eg anterior spinal A occlusion.

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36
Q

Mechanisms of altered conciousness

A

Metabolic disturbance
RICP pressure on brainstem inhibits RAS
Brainstem lesion eg infarct

37
Q

Different states of varying conciousness

A
  • reduced wakefulness- REM, sleep
  • reduced awareness- acute confusion, PVS
  • both reduced- coma anaesthesia.
38
Q

Causes of reduced conciousness

A

-IC-
Haemorrhage, stroke, CA, RICP, infection, trauma, epilepsy.
-EC-
Hypoxia, electrical, metabolic, sepsis, toxin, endocrine.

39
Q

Posturing

A

-decerebrate-legs ext, arms ext. WORSE.
Upper brainstem brainstem damage. Below red nucleus.
-decorticate-leg ext, elbows flex
CST damage. 1st if herniation.

40
Q

GCS

A

-E (4)-
No eye opening, open to pian, open to voice, open spontaneously.
-V (5)-
None, incomprehensible, inappropriate, confused, orientated.
-M (6)-
None, extension to pain, flexion to pain, withdrawal from pain, localisation of pain, obey commands.

41
Q

Locked in syndrome

A

Lesion just belwo mid pons RF.
Alert and awake but mute and quadriplegic.
CN III often intact.

42
Q

Reticular formation

A

Specialised interneurones in brainstem.

RAS part is devoted to arousal. Regulated by sensory and cortical inputs. Outputs to thalamus, hypothalamus, BFN, SC.

43
Q

REM sleep

A

Arousal beta waves but strong thalamic inhibition.
Decending LMN inhibition by glycinergic RF fibres via RSTs. Not EO muscles, and some CN function.
Autonomic- erection and loss thermoregulation.
Essential for life.

44
Q

Sleep function

A

Energy conservation and repair
Memory consolidation
Clear EC debris
CNS reset

45
Q

Sleep disorders

A

Insomnia eg anxiety cortical stimulation.
Narcolepsy loss orexinergic visual input to RF.
Apnoea eg obese. ChemoR to thalamus= wake.

46
Q

RF nt’s

A

Glutamate to thalamus
Histamine to hypothalamus
ACh to BFN
Postive feedback loop.

47
Q

CT indications in head trauma

A

-CT head less than 1 hour if-
GCS under 13 initially, under 15 after 2 hours.
Suspect open or depressed skull fracture, signs of basal fracture.
Post trauma seizure, focal neural deficit, more than 1 vomit.
-less than 8 hours if-
Age over 65
Hx of bleeding disorder
Dangerous MOI
Over 30 mins retrograde amnesia.

48
Q

Extradural haemorrhage

A 
Arterial
Bewteen skull and dura
High impact
Initally regain conciousness then decline. 
Blood not beyond sutures 
Usually in young
Can get herniation
Decrease GCS
Surgery if large otherwise wait. 
Often skull fracture ans MMA cause.
49
Q

Subdural haemorrhage

A

Venous
Between dura and arachnoid
Acute, subacute (3-7d), chronic (2-3wk after injury).
Spreads beyond sutures, not dural reflections.
Young acute trauma, elderly small injury can cause chronic.
Acute= reduced conciousness and pupil defect.
Crescent CT- acute bright, chronic dark.

50
Q

SAH high mortality

A 
Arterial
Between pia and arachnoid
Trauma or spontaneous (aneurysm or AVM).
Thunderclap, neck, stiff, vomit, photophobia, NOT FEVER. 
CT white star around circle of willis.
LP for CSF blood if no RICP. 
RFs- CT disease, HTN, alcohol. 
Berry aneurysm in 80%. A/MCA branching points. 
Screen if family hx or risk occupation.
51
Q

IC haemorrhage bleed in brain tissue

A

Can be trauma. Usually spontaneous anaerysm or tumour.
S+S depend on site.
Surgery possible.

52
Q

Diffuse axonal injury acceleration/deceleration.

A

Shear at WM/GM junction.
Instant LOC then PVS.
Need MRI.
Mx- prevent secondary damage due to cerebral oedema and hypoxia.

53
Q

Skull fracture

A

CSF rhino and otorrhoea. Dural tear risk meningitis.
CSF tests- filter paper, glucose dip, B2 transferrin.
Base skull fracture- periorbital ecchymosis, battles mastoid, CSF rhino and otorrhoea.

54
Q

RICP

A

Over 20mmHg for over 5 mins. Normal is 5-15.
Herniation- cingulate gyrus, uncus, cerebellar tonsils.
ICP variation- AP (HR), VP (IT pressure, gravity).
Monro kellie- total brain+ blood+ CSF volume constant.
Compensated- mass= reduce CSF and venous volume, brain atrophy.
Positive feedback peripheral constriction and brain dilation.
LP= coning.

55
Q

RICP symptoms

A

Bilateral ache, variable onset, no radiation.
Nausea, loss vision, altered mental state.
Worse lying down and bending forward as increase IT pressure.
Better if sit/stand.
Worse first thing in morning.
-RED FLAGS-
Focal neurology/cognition/visual change, seizure, syncope.
Neck stiff, fever, rash, vomit.
Headaches wake them up.
Head injury last 90 days.
New headache if hx CA, immunosuppression.
Thunderclap.
Change headache with posture or exertion.
New or changed heache if over 50 or under 5yo.

56
Q

RICP signs

A

Papilloedema- reduced axoplasmic flow.
CN III palsy- uncal herniation.
CN VI palsy- long course.
Loss vestibulochoclear reflex- brainstem death.
Also reduced cognition, irritability, low GCS, UMN signs, decorticate or decerebrate, cushings triad (irregular respiration, bradycardia, systemic HTN/wide PP).

57
Q

RICP causes

A
  • blood- extra/subdural, SAH, IC.
  • brain- tumour, oedema (trauma, infarct, malignancy, infection, water toxicity).
  • CSF- hydrocephalus (acquired, congenital, NPH).
  • other- meningioma, abcess, IIH.
58
Q

Hydrocephalus

A

Increase production rare- choroid plexus papilloma.
Reduced flow- spina bifida, duct stenosis, clot post IVH, SOL.
Reduced absorption- obliterative arachnoiditis post bleed/trauma.
Congential- skull not fused.
-complications- neurological deficit, infection, epilepsy, chronic RICP.
-mx- induce coma, osmotherapy, maintain bm, antipyretic, hypothermia, elevate head, dexamethasone, acetazolamide (reduce CSF production). Surgery- decompression craniotomy, shunts.

59
Q

Drug neuro ADRS

A
  • ataxia- phenytoin, carbamazepine, lithium.
  • seizure- TCA, clozapine.
  • headache- GTN, sildenafil.
  • myopathy- statin, CS.
  • parkinsonism- neuroleptics.
  • peripheral neuropathy- chemo, metronidazole.
  • tremor- beta agonist, lithium, valproate.
60
Q

MSE

A 
Appearance and behaviour
Speech
Mod
Thoughts
Perceptions
Cognition
Insight
61
Q

Association areas

A

-parieto-occipito-temporal:
Integrates visual, proprioceptive and auditory inputs to understand immediate surroundings.
-wernickes- comprehend language.
-pre frontal- integrates sensory and motor= consider plan and consequences. Contains brocas- thoughts to words.
-limbic- emotional connotations to input/behaviour. Reward and punishment.

62
Q

Frontal lobe MICCES

A 
Motor 
Inhibition
Cognition
Continence
Eye movement
Speech
63
Q

Parietal lobe C BEVS

A 
Calculation and writing
Body image
External environemnt (hemineglect)
Visual projections
Sensory
64
Q

Temporal lobe MOSHEV

A 
Memory
Olfaction
Speech comprehension
Hearing
Emotion
Visual projections
65
Q

Dominance

A

Dominant usually L- sequential processing eg language, maths, logic.
Non dominant- whole picture processing eg body image, visuospatial, emotion, music.

66
Q

Cut corpus callosum

A

Visual decussation in optic chiasm. Language L hemisphere.
So show image in R field-can say what see.
But sensory decussation SC and medulla so L hand tough= R hemisphere ID object BUT cant communicate with L to say what feel.

67
Q

Speech path

A

Auditory/visual/cortical input to wernickes superior temporal.
Arcuate fasciculus WM to brocas inferior lateral frontal lobe.
To motor cortex to produce speech.

68
Q

Wernickes fluent aphasia

A

Nonsense

69
Q

Brocas aphasia

A

Non fluent

But they understand

70
Q

Memory

A

Declarative through cortex. Hippocampus consolidation.
Non declarative cerebellum and basal ganglia.
Neurplasticity- increase nt each AP, increase post synaptic Rs, increase branches to axon and multiple terminals.

71
Q

Anterograde amnesia

A

Of new memories.

Temporal hippocampal gyrus lesion.

72
Q

retrograde amnesia

A

Of old memories. Less common.

Damage cortex eg dementia.

73
Q

Alzheimers

A

MRI general atrophy, disproportionate in hippocampus.
SPECT for activity.
-pathology-
Abnormal protein build up in brain- amyloid plaque and tau hyperP tangles.
Reduced nt’s
Loss of connections
Death of neurones and brain tissue.
-tx-
AchE inhibitors for mild to moderate disease. Eg donepezil, rivastigmine.
AE- headache, GI, drowsy, urinary retention, seizure, bradyc.
Memantine NMDA R antagonist for severe AD.
AE- drowsy, dizzy, constipation, headache, SOB, hallucination, confusion, vomit, gait.
- antipsychotics and sedation last resort-
Antipsychotics CVS risk and falls with benzo. Infection risk. And stiffening in lewy body dementia.
Start low, IM< motor closely and ST only.

74
Q

Vascular dementia

A

Sudden stepwide deterioration.
Stroke related. Subcortical. Often mixed with AD.
Less memory loss early on.
-symptoms- planning, processing speed, following steps, concentration, confusion, language, visuaspatial, memory, apathy, depression, anxiety.
-tx- control CVS RFs.

75
Q

Fronto temporal dementia -picks disease

A

Abnormal protein build up- lewy bodies.
-symptoms- loss inhibitions, loss interest, loss sympathy and empathy, OCD, cravings, speech problems, word meaning, agnosia.
No tx.

76
Q

Lewy body dementia

A

Symptoms-
Reduced alertness, hallucination, delusion, movement and sleep disturbance
No specific tx- donepezil and rivastigmine can reduce pyschotic symptoms.

77
Q

CJD prion

A

Sporadic in over 40s.
NvcJD BSE younger.
-symptoms- memory, moos, reduced interest, clumsy, slurred speech, dysarthria, hypertonia, incontinence, paralysis.
Die in 6 months!

78
Q

Neuro infection

A

Direct from mid ear or base skull fracture.
Blood- spesis or endocarditis.
Iatrogenic- VP shunt, surgery, LP.

79
Q

Meningitis causes

A

Affects leptomeninges (pia and arachnoid). Possible spetacaemia.

  • neonate- ecoli, listeria mnocytogenes group B strep.
  • 2-5- H influ B, strep pneumoniae, N meningitidis
  • 5-30- N meningitidis, strep pneumoniae.
  • over 30- strep pneumoniae. N monocytogenes over 60.
  • immunocompromised- staph, grey eg enteric, Pa
80
Q

Encephalitis viral parenchyma infection

A

Neurone death by inclusion bodies- CMV
Temporal lobe herpes.
SC MNs polio
Brainstem rabies

81
Q

SOL

A

Local destruction
Midline shift
Herniation

82
Q

Subfalcine herniation

A

Same side as mass.
Cingulate gyrus under falx cerebri free edge.
Compress ACA so frontal, parietal and CC ischameia.

83
Q

Tectorial herniation

A

Uncus/medial parahippocampal gyrus through tectorial notch.
Damage ipsialteral CN III.
Occlusion PCA and superior cerebellar A.
Secondary haemorrhage to brainstem fatal.

84
Q

Tonsillar herniation

A

Cerebellar tonsils through FM.

85
Q

Brain tumours

A

Benign eg meningioma.
Malignant eg astrocytoma.
Other eg neurofibroma, medulloblastoma, lymphoma, mets (most common).

86
Q

Stroke

A

-Cerebral infarction 85%
Embolism most common.
Regional to 1 cerebellar A.
Lacuna- under 1cm, associated HTN, basal ganglia affected.
-Haemorrhage 15% (IC 10%, SAH 5%)
IC- HTN damage, charcot bouchard aneurysm, amyloid angiopathy, inherited, SOL.
SAH- berry, male, HTN, atheroma.

87
Q

Pupillary changes

A

Small, reactive- endoc
Large, fixed- brainstem death
Fixed, dilated, ptosed- 3rd N palsy.

88
Q

Normal press hydrocephalus
Excess CSF but normal press
Triad px

A

Dementia
Urin incontin
Abn gait

causes of signs (13 decks)

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