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Spinal Pathology Flashcards

1
Q

What is the difference between nerve regrowth in the PNS and CNS?

A

The PNS can regenerate following injury, while the CNS does not regenerate after injury in adults.

PNS growth is guided by growth cones and the environment, while CNS neurons are inhibited by factors in the adult CNS.

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2
Q

Define Bell’s Palsy.

A

Acute unilateral facial nerve weakness or paralysis of rapid onset (less than 72 hrs) and unknown cause.

It primarily affects the muscles of facial expression.

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3
Q

What are some potential causes of Bell’s Palsy?

A
  • HSV
  • Varicella zoster virus
  • Autoimmunity
  • Birth trauma
  • Inflammation and edema of the facial nerve
  • Compression of the facial nerve
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4
Q

List some risk factors for Bell’s Palsy.

A
  • Pregnancy
  • Obesity
  • Diabetes
  • Hypertension
  • Immunocompromised states
  • Upper respiratory conditions

These risk factors can increase the likelihood of developing Bell’s Palsy.

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5
Q

What are the signs and symptoms of Bell’s Palsy?

A
  • Rapid onset facial muscle weakness
  • Drooping of the eyebrow and corner of the mouth
  • Incomplete eye closure
  • Ear/postauricular pain
  • Changes in taste
  • Speech problems
  • Hyperacusis

Symptoms can vary in presentation and severity.

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6
Q

What is diabetic neuropathy?

A

A common complication of T1 and T2 diabetes resulting in progressive distal sensorimotor polyneuropathy.

It can manifest as symmetrical sensory loss and motor weakness.

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7
Q

What are the main risk factors for diabetic neuropathy?

A
  • Prolonged exposure to high blood glucose levels
  • Poor glycemic control
  • Age
  • Hypertension - microvascular disease
  • Dyslipidemia - nerve damage
  • Smoking - vasoconstriction
  • Alcohol use - toxic on nerves

These factors contribute to nerve damage and dysfunction.

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8
Q

Describe the typical presentation of diabetic neuropathy.

A
  • Symmetrical stocking and glove distribution
  • Bilateral numbness
  • Tingling or burning sensation
  • Muscle weakness and atrophy
  • Autonomic symptoms (gastroparesis, erectile dysfunction, orthostatic hypotension, neurogenic bladder)
  • pain - persistent and worse at night

Symptoms progress proximally and can lead to increased risk of falls.

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9
Q

What is the prognosis for diabetic neuropathy?

A

Usually unable to reverse, but treatment can help slow progression and decrease symptoms.

Patients often have a reduced life expectancy by three years compared to those without the condition.

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10
Q

What is motor neuron disease?

A

A group of neurological disorders that progressively damage parts of the motor nervous system, eventually resulting in death.

ALS (Amyotrophic lateral sclerosis) is the most common form.
Progressive bulbar palsy is the second most common - muscles of talking and swallowing.

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11
Q

What is the prognosis for ALS?

A

Survival from diagnosis is around 3 to 5 years.

Prognosis can vary based on the patient’s age and symptom onset.

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12
Q

Define multiple sclerosis.

A

Chronic degeneration of the myelin sheath surrounding neurons in the CNS with an autoimmune component.

It involves inflammation, demyelination, and axonal degeneration.

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13
Q

What are the types of multiple sclerosis?

A
  • Relapsing and remitting
  • Secondary progressive
  • Primary progressive

These types differ in their progression and recovery patterns.

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14
Q

What is the hallmark of multiple sclerosis symptoms?

A

Symptoms appear at different times and locations, typically acute/sub-acute with periods of variable remission.

This variability can complicate diagnosis.

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15
Q

What is myasthenia gravis?

A

An autoimmune disease that targets the neuromuscular junction (NMJ).

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16
Q

What are the signs and symptoms of myasthenia gravis?

A
  • Progressive muscle weakness
  • Bulbar muscle weakness
  • Ocular symptoms (ptosis, diplopia)

Symptoms typically improve with rest. Worse at night, worse on exertion

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17
Q

What is the role of acetylcholine in myasthenia gravis?

A

Autoantibodies block acetylcholine from binding to receptors at the NMJ, preventing muscle contraction.

This leads to the characteristic weakness seen in the condition.

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18
Q

What are the main autoantibodies associated with myasthenia gravis?

A

Anti-AChR (85%), Anti-MUSK (up to 15%), Anti-LRP4 (small percentage)

These autoantibodies interfere with neuromuscular transmission.

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19
Q

What imaging studies are used to rule out thymoma in myasthenia gravis patients?

A

Chest CT or MRI

Thymoma is a tumor of the thymus gland, which can be associated with myasthenia gravis.

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20
Q

What is the purpose of the Edrophonium test?

A

To assess for rapid and transient improvement in muscle strength after IV administration of edrophonium
Positive can indicate myasthenia gravis

Edrophonium is a short-acting acetylcholinesterase inhibitor.

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21
Q

What is the mechanism of action of Neostigmine/Pyridostigmine in myasthenia gravis treatment?

A

They are acetylcholinesterase inhibitors that increase the concentration of acetylcholine in the neuromuscular junction

This helps to outcompete autoantibodies.

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22
Q

What is the role of Prednisolone in managing myasthenia gravis?

A

It is a glucocorticoid = immunosuppressant = reduces inflammation hence autoantibody production and muscle degeneration

Administered at low doses to suppress the immune response.

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23
Q

What is the treatment for severe acute exacerbations of myasthenia gravis?

A

IV immunoglobulins

They neutralize autoreactive antibodies and cytokines.

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24
Q

What are common complications of myasthenia gravis?

A

Disability, impaired vision, poor speech, compromised swallow, myasthenic crisis

Myasthenic crisis is life-threatening and affects respiratory muscles causing potentially fatal difficult breathing

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25
Q

What is the prognosis for most patients with myasthenia gravis?

A

Good symptom management and maintenance of normal or near-normal quality of life

Myasthenic crisis can be fatal if not promptly recognized.

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26
Q

What is the epidemiology of myasthenia gravis?

A

1.5 per 100,000, commonly affects individuals aged 30-40

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27
Q

Define varicella zoster.

A

Contagious virus responsible for chickenpox and shingles

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28
Q

What are the risk factors for severe varicella infection?

A
  • Numerous lesions = more severe disease
  • Adults (including pregnant women)
  • Immunocompromised individuals
  • Exposure to infected individuals - vesicular fluid or airborn droplets

Reactivation risk factors include age and weakened immune system.

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29
Q

What are the signs and symptoms of chickenpox?

A
  • 10-20 day incubation period
  • Mild fever, malaise, myalgia
  • Erythematous pruritic macules and papules
  • Crusts form after pustules

Lesions typically heal within 7-10 days. Are very itchy at start of disease. Lesion more common on scalp, face, then trunk and extremities

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30
Q

What is the pathophysiology of varicella zoster virus infection?

A

Primary infection causes chickenpox, usually self limited in otherwise health children. Affected individual in contagnous via airborne droples and contact with vesicular fluid (until lesions crusted over). Initial infection is in the upper airways, then spreads into the blood stream. Virus becomes dormant in dorsal root ganglia - 98% of adults are seropositive.

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31
Q

What is the treatment for high-risk individuals exposed to chickenpox?

A

Two-stage vaccination program

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32
Q

What is shingles?

A
  • Reactivation of varicella -most common in individuals with CD4 count less than 200.
  • Painful vesicular eruption in dermatomal distribution + dyesthesia
  • Potential for acute retinal necrosis is eye involvement
  • Mostly thoracic dermatomes
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33
Q

What is postherpetic neuralgia in the context of shingles?

A

A complication of shingles characterized by persistent pain after the rash has healed

It is more common in immunocompromised individuals.

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34
Q

What is the epidemiology of chickenpox in the US?

A

95% of adults have been infected, most commonly affects children under 10 years

10% of those infected will later develop shingles.

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35
Q

Define denervation atrophy.

A

Grouped atrophy of muscle fibers that have lost innervation from shared lower motor neuron

Causes include traumatic nerve injury and diseases like ALS.

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36
Q

What are some complications of Bell’s palsy?

A

eye injury (corneal ulceration, vision loss)
facial pain
dry mouth,
intolerance to loud noises
abnormal facial muscle contraction during voluntary movements (unusual reinnervation of the facial nerve during recovery), psychological sequelae.

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37
Q

What investigations should be done for a patient with Bells Palsy?

A

diagnosis is made when no other medial condition is found, requires urgent referal is suspect upper motor neuron lesion, cancer, acute system or severe local infection, trauma.

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38
Q

What treatment should be offered for Bells Palsy?

A

Eye lubricating drops for the affected eye and ointment at night, tape shut at bedtime,
If present within 72hrs should be given prednisolone, may give antiviral alongside corticosteroid.
If difficult with chew/swallow recommend use of straw/avoid soft foods - may put on thick fluid diet

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39
Q

What is the prognosis of Bellsy Palsy?

A

Improvement within 3 weeks, complete recovery at 3 months, varies based on degree of paralysis, age and if pregnant (older, higher severity and pregnancy = worse), 6.5% of Bells palsy cases reoccur

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40
Q

What is the relevant epidemiology of Bells Palsy?

A

Common between 15 and 45 years. Rare one case every 2 years in GP.

41
Q

What is the basic pathophysiology underpinning diabetic neuropathy?

A

Chronic hyperglycemia triggers metabolic changes, including an increase in polyol pathway flux, accumulation of advanced glycation end products (AGEs) (causing inflammation and apoptosis, activation of PKC - which disrupts nerve structure and function.
Diabetes causes small vessel disease - leading to nerve ischemia and hypoxia.
Autoimmune response against neuronal antigens - leading to demyelination and axonal degeneration
Chronic low grade inflammation - direct neuronal damage
Oxidative stress from hyperglycemia damages nerves directly and promotes inflammation.

42
Q

What investigations should be done for suspected diabetic neuropahty?

A
  • Blood tests - FBC, Renal function, liver function, thyroid funcation, VB12, HbA1c - rule out differenaites such as VB12 deficiency and hypothyroidism which can mimic
    *Urinalysis - microalbuminuria - early neuropathy
    *Nerve conduction studies - gold stand for confirming peripheral neuropathy - measure the speed of conduction - slow conduction velocity or reduce amplitude of action potentials
    *Quantitative sensory testing - focus on large fibres for vibration and thermal funcation - early sensory dysfunction
    *Skin biopsy - measure nerve fibre density.
43
Q

How does diabetic neuropathy present on histological slides?

A

Diffuse loss of darkly stained thickly and thinly myelinated fibres, also microvascular disease with thickened walls of small vessels.

44
Q

What are some common complications of diabetic neuropathy?

A

risk of foot uclers - requires competent foot and lower limb examination. Should be given protective footwear. Peripheral Vascular Disease. Cardiovascular autonomic neuropathy.

45
Q

What is the recommended treatment for diabetic neuropathy?

A

glycaemic control to prevent progression, symptomatic pain relief (tricyclic antidepressants, SNRI ), or targeted dysfunction (gastroparesis/erectile dysfunction)
Should be given advice to maintain a healthy weight, regular exercise and stop smoking and psychological support for chronic pain

46
Q

What is the relevant epidemiology of diabetic neuropathy?

A

affects 50% of diabetics, most common diabetic complication, often occurs in late adulthood. More common in type 2 diabetes.

47
Q

What is the aetiology of ALS?

A

30 genes implicated, polygenic with high environmental influence, familial patterns, mutated genes tends to be involved in cellular metabolism such as mitochondrial funcation, RNA metabolism, DNA repair etc. Some are specific to neurons including causing glial dysfunction and axonopathy. Effects motor neurons most due to higher metabolic rate.

48
Q

What are the risk factors for ALS?

A
  • Family history (5-10% of cases), smoking, exposure to heavy metals and pesticides, elite athletes (particularly in contact sports with repeat concussions), males more likely to develop at a younger age
49
Q

What is the basic pathophysiology of ALS?

A

Genetic mutation combined with environmental factors results in metabolic dysfunction and apoptosis of motor neurons. Progressive disease destroying both upper an dlower motor neurons. The sensory neurons are spared. Characterised by protein aggregates accumulating in the neuron - contributing to neural deregulation.

50
Q

What are the signs and symptoms of ALS?

A

lower motor neuron symptoms (disuse atrophy, hypotonic, hyporeflexia, fasiculation) then develops into upper motor neuron symptoms (hypertonia, spastic paralysis, hyperreflexia, no fasiculation, positive Babinski sign).
This is gradual, first reported in upper limbs. Patients complain of increased fatigue when exercising, clumsiness, dropping things, falls or slurred speech.
In more severe have reduced respiratory function such as excessive daytime sleepiness aand SOB when lying down.
Often associated with cognitive decline - behavioural changes, emotional lability and frontotemporal dementia.

51
Q

What treatment is often offered for ALS?

A

No effective treatment.
Riluzole - slow progression and extend survival by several months
Non-invasive ventilation - support breathing when respiratory muscles weaken.
Quinine first line, baclofen second line for muscle spasticity and anti-muscarinic for excessive saliva.
Exercise programmes - maintain range of movement, prevent contractures, reduce stiffness and discomfort.
Benzodiazepines - reduce breathlessness worsen by anxiety
Advanced directives - to document wishes as disease progresses
Special technology adaptation - communication devices etc.
End-of-life care - thickened fluid diet, pain relief, psychological support, constipation etc.

52
Q

What is the most common complication from ALS?

A

Death from respiratory failure or pneumonia

53
Q

What is the relevant epidemiology for ALS?

A

Rarely presents before 40 years, are often later middle-aged norm with an affected relative. Disproportionately high prevalence in elite sport athletes.

54
Q

What is the aetiology of MS?

A

multifactorial in nature, 15-20% FH (HLA genes), EBV exposure 5.5 times higher risk (molecular mimicry), smoking, Vitamin D deficiency,

55
Q

What are the key risk factors for MS?

A
  • Genetic (mutants in HLA region), previous viral exposure particularly Epstein-Barr virus, female, lower relapses in pregnancy, more relapses in post-partum.
56
Q

What is the key pathophysiology of MS?

A

Key idea - a combination of genetic nd environmental factors lead to an autoimmune disease causing inflammation, demyelination and axonal degeneration in the white matter of the CNS - targets antigens in the myelin sheath. Areas of demyelination are called ‘plaques’, as inflammatory infilates of mononculear cells and lymphocytes accumulate. Surrounding areas suffer from interstitial oedema in acute stage. Initially only myelin destruction with relative axon preservation, rarely some patients may have remyelination allowing some functional recovery, in chronic disease axons and cell bodies may be lost.

57
Q

What are the key signs and symptoms of MS?

A

Dependent on where the nerve damage happens. All are CNS. Includes vision, sensation, coordination, movement, bladder or bowel control.
Hallmark - symptoms appear at different times and location, norm acute/sub-acute with form form of variable remission before recurrence.

Most common locations of lesions include spinal cord (50%), optic nerve (25%) and brainstem/cerebellum (20%).

58
Q

How is the spinal cord affected in MS?

A

Can have spinal cord lesion - transverse myelitis.
Focal inflammation within the cord - paresthesia or weakness below level of lesion, develops over hrs/days
Urinary symptoms etc
Aligns with a partial spinal cord lesion signs and symptoms.

59
Q

How is vision commonly affected in MS?

A

Optic neurtitis = unilateral vision loss with central scotoma (area o f loss with blurry edge) and pain on ocular movement

60
Q

What are the features of the different types of MS?

A

Relapsing and remitting - clear relapses with full or partial recovery. Relapses are more common in early disease. No disease progression between relapses. 85-90% of initiall cases
Secondary progressive - starts with relapsing-remitting picture than eact successive relapse becomes less complete. Disease progresses between relapses causing long-term disability. Occurs in 40%
Primary progressive - disability worsening gradually from onset without true relapses or remission, cumulative onset. 10-30% of patients present with this form.

61
Q

What criteria is the diagnosis for MS based on?

A

Revised McDonald criteria

62
Q

How can an MRI show MS?

A

shows white matter disease, hyperintense lesions on T2 weighted images particularly in the pariventricular area, the corpus callosum and juxtacortical white matter in the brain. May have widespread abnormalities at presentation with symptoms isolated to one/two sites - indicates lesions at different times - important criteria in MS diagnosis.

63
Q

How is MS diagnosed?

A

MRI - white matter lesions (see card)
Cerebrospinal fluid examination - increase lymphocyte cell count, oligoclonal bands (intense bands when stating for IgG on western blotting) in CSF but not serum is highly suggestive of MS.

64
Q

What treatment is recommended in long term MS?

A

DMARDs
Natalizumab - antagonises alpha4-beta-1-integrine found on surface of leucocytes.
Beta-inteferon - immunomodulator that reduces inflammation.

Chronic management - symptomatic relief - including fatigue, spasticity, ataxia/tremor, mobility, mental health, pain, sexual problems and bladder problems.

General treatment: care of consultant neurologist and a MDT.
Conservative - regular exercise, smoking cessation, annual review in secondary care, provide information of advance care planning/power of attorney, end of life care.
Medical - management of co-morbidities such as diabetes.

65
Q

What treatment is recommended in MS relapse?

A

In a relapse short course of high-dose corticosteroids - oral methylprednisolone 0.5g daily for 5 days - within 14 days of onset of symptoms.

66
Q

What is the prognosis like for MS?

A

Overall life-expectancy is disease by6/7years compared to general population. Require cane 28yrs after diagnosis. Priamry progressive has a worse prognosis, whilst relapse-remission tends to have low disability by ten years.

67
Q

What is the key epidemiology of MS?

A
  • 150 per 100,000 in the UK, usually amongst white adults with peak onset of replase-remitting form of the disease being between 20-30years, this may then convert to secondary-porgressive at 40-44yrs. More common in females. Often have a history of previous neurological symptoms.
68
Q

What are the risk factors for Myasthenia Gravis?

A

female, history of autoimmune disease (RA, MG etc), genetic markers (HLA-B8), thyroid disease, pregnancy, infections can exacerbate.

69
Q

What is the pathophysiology of myasthenia Gravis?

A

type 2 hypersensitivity reaction
Failure of central and peripheral tolerance mechanism results in IgG Autoanitobodies:
Anti-AChR - Competitive antagonist of AChR, prevents ACh binding to R at the NMJ leads to lack of muscle contraction.
Anti-MUSK - prevents the formation of mature AChR on the neural membrane
Anti-LPR4 - prevents mature NMJ formation
Internalisation and degradation of receptors, activation of complement which damages the postsynaptic membrane.

70
Q

What investgiations help diagnosis myasthenia gravis?

A

Nerve conduction studies - reduced conduction speed, reduced amplitude in compound muscle action potentials on further on repeated stimulation. Also single-fibre electromyography - most sensitive - idneitfies variable time and failure of individual fibres to respond to stimulation.
ICe pack test - ask to hold cold cold cloth over eyelid - will reduce eye lid drooping
Bloods - elevated wbcs. Looks for specific auto-antibodies Anti-AChR (85%), Anti_MUSK (up to 15%) and Anti_LRP4 - small percentage of patients.
Chest CT/MRI to rule out thymoma or thymic hyperplasia.
Edrophonium test - bedside - IV administration of adrophonium a short acting Achesterase inhibitor - pos if rapid and transient improvement in muscle strength after injection.

71
Q

What treatment is used for varicell zoster virus?

A

People at high risk of getting ill from chicken pox and their close contacts can receive a two stage vaccination programme.
Antiviral medication (within first 24hrs), paracetamol
Shingles - antiviral tends to be aciclovir, NSAIDs, amitriptyline, oral corticosteroids

72
Q

What are the signs of an upper motor neuron lesion?

A

Hyperreflexia
Hypertonia
Pos. Babinski sign
some loss in muscle mass.

73
Q

What are the signs of a lower motor neuron lesion?

A

Hyporeflexiva
Rapid muscle atrophy
Hypotonia
Negative babinski sign

74
Q

What are the key pyramidal motor spinal tracts to be aware of?

A

Corticobular - voluntary movement of the head/neck
Corticospinal - lateral to the limbs, medial to the trunk - voluntary movement.

75
Q

Provide a summary of the corticospinal tract

A

Synapse with a lower motor neuron in the ventral horn in the spinal cord.

76
Q

Provide a summary of the corticobulbar tract

A

Originate in S1
Pass through genu of internal capsule
Synapse with CN3,4,5,6 - bilaterally,
7 - upper part bilaterally and lower part contralateral
9,10,11 (cranial) - nucleus ambiguus - bilateral
12 - hypoglossal - contralterally??

77
Q

What is the clinical relevance of lesions in the corticobulbar tract?

A

CN7 - upper motor neuron lesion e.g stroke if forehead sparing and lower motor neuron lesion is not
CN12 - tongue deviates towards the side of the lesion - Right hypoglossal nerve lesion - innervates left side of tongue - deviates to the right. **

78
Q

Provide a summary of the DCML pathway

A

Responsible for fine touch, proprioception, vibration and pressure
Ascending pathway
Cell body in DRG
Ascends in DC - fasiculus cuneate (UL) or fasiculus gracilis (LL)
Synapse in medulla (Nucleus cuneatus UL or nucleus gracilis LL)
Medial lemniscus fibres desiccate to the contralateral side.
Synapse in VPL nucleus of the thalamus
Synapse in S1

79
Q

Provide a summary of the spinothalamic pathway

A

Responsible to conscious pain, temp and crude touch
Ascending pathway
Cell body in the DRG
Synapse in dorsal horn
Desciate via the anterior white commisure
Ascend in the spinothalamic tract
Synapse in the VPL nucleus of the thalamus
Pass through the posterior limb of the internal capsule
Synapse in S1

80
Q

Provide a summary on the vestibulospinal tract

A

Descending tract
Vestibular sensation input from CN8 to cerebellum, medial vestibular nucleus (pons) and lateral vestibular nucleus (medulla)
Cerebellum can communicate back and forth with the medial and lateral vestibular nucleus
Medial nuc -> medial vesibulospinal tract -> LMNs of the head and neck (vestibulocolic reflex)
Lat nuc -> lateral vestibulospinal tract -> LMNs of the trunk and limbs. (vestibulospinal reflex)
Helps maintain balance and posture

81
Q

Provide a summary of the tectospinal/bulbar tract

A

Descending tract
Sends motor signals to co-ordinate head/neck (tectobulbar) and body movements (tectospinal) with visual stimuli (superior colliculi) and auditory(inferior colliculi) respectively
Located over the roof of the cerebral aqueduct the colliculi are termed the tectum.

82
Q

Provide a summary of the reticulospinal tracts

A

Responsible for subconscious motor control e.g breathing
Medullary reticular formation - stimulates flexor inhibits extensor
Pontine reticular formation - > autonomic function, stimulate extensor/

83
Q

What spinal tracts are located int eh dorsal funiculus of the spinal cord.

A

The dorsal columns
This includes the gracile fasiculus medially - for the lower limb - light touch, vibration and propriocpets
And the cuneate fasiculus laterally for the upper limb.

84
Q

What tracts are located in the lateral funiculus of the spinal cord?

A

The lateral corticospinal
The anterolateral system (pain)
The spinocerebellar tract - tension (unconscious proprioception from lower body proprioception)

85
Q

What spinal tracts are located in the ventral funiculus?

A

The ventral corticospinal - vol mov to trunk
Extrapyramidal tracts (tectospinal, vestibulospinal) - reflexes and balance.

86
Q

Label the pink tracts

A

Lateral and anterior corticospinal

87
Q

label the green tracts

A

The dorsal and ventral spinocerebellar (tension/propricopection)

88
Q

label the orange tracts

A

The DCML
The cuneate and gracile fasiculus

89
Q

Label the purple tract

A

The anterolateral system (STT)

90
Q

Label the red tracts

A

The pontine and medullary reticular formation

91
Q

Label the black tract

A

The tectospinal tract

92
Q

Label the grey tract

A

The vestibulospinal tract.

93
Q

How does central cord syndrome present?

A

Loss of ventral horn, AWC
Loss of pain and temperature at level of lesion bilaterally as unable to desciate in the AWC
May expand to involved the upper limb regions of the corticospinal and STT tract.
Pain and temp from level below the lesion are preserved as already dedicated to the peripheral white matter.
Touch and Position are preserved at and below the level of the lesion as do not need to cross the centre of the spinal cord.

Norm cause - hyperextension of the neck

94
Q

How does posterior column syndrome of the spinal cord present?

A

Loss of DCML - position and fine touch lost at and below the lesion
Motor function and pain sensation preserved.

95
Q

How does anterior spinal artery syndrome present?

A

One anterior artery supplies the lateral and ventral funiculus
Loss of motor function and pain sensation below the injured segment
Conscious proprioception and fine touch (DCML remain)

96
Q

How does Brown sequard syndrome present?

A

Damage to one half (left/right) of the spinal cord in its entirety.
Ipsi side of lesion - Loss of motor function, loss of fine touch/proprioception
Cont side of lesion - loss of pain and temperature.

97
Q

What is the role of the pain dorsal column pathway?
How can this be utilised clinically?

A

Belief that visceral pain is transmitted along the dorsal column pathway rather than the anterolateral system
Apply a lesion to the dorsal column close to the midline - can reduce transmission up these tracts - reduce chronic pain from the viscera.

98
Q

What is the difference between a Duchenne and a pyramidal smile?

A

Duchenne = real smile = oriringates from the emotional expression centres such as the anterior cingulate gyrus motor area or the hypothalamus
Pyramidal = fake = originate from M1
Both affect motor neuron in the facial nucleus for a smile
However the Duchenne smile also have ocular involvement => scrunching of eyes.

SPINE (20 decks)

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