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MBBS - Y1 > Week 14 - gait and limp > Flashcards

Week 14 - gait and limp Flashcards

1
Q

What are the two phases of a normal gait? (LO1)

A
  • Stance - 60% of walking.

- Swing - 40% of walking.

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2
Q

What are the four parts of the stance phase in normal gait? (LO1)

A
  1. Heel strike to foot flat.
  2. Foot flat to midstance.
  3. Midstance to heel off.
  4. Heel off to toe off.
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3
Q

What are the two parts of the swing phase in normal gait? (LO1)

A
  1. Acceleration to midswing.

2. Midswing deceleration.

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4
Q

Describe antalgic gait. (LO1)

A
  • Another name for limp.
  • Shortening in stance phase relative to swing phase.
  • Prevents an area that is painful from being put under too much pressure.
  • Reason for this could be traumatic, infectious, inflammatory, vascular or neoplastic.
  • The likelihood of developing antalgic gait increases with age.
  • More than 60% of people >80 are affected.
  • Treatment and management will depend on diagnosis as fixing the underlying issue is key. Refer to the appropriate specialist.
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5
Q

How do we diagnose the cause of an antalgic gait? (LO1)

A
  • Comprehensive history.

- Examination of the lower limb, hip and spine.

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6
Q

List the differential diagnoses for antalgic gait. (LO1)

A

Traumatic:

  • Fracture or sprain of the lower extremity.
  • Vertebral body fracture.
  • Hip fracture.

Infectious:

  • Epidural abscess.
  • Osteomyelitis.
  • Discitis.
  • Septic arthritis.

Inflammatory:

  • Gout.
  • Lumbar radiculopathy.
  • Sciatica.
  • Bursitis of the hip or knee.
  • Rheumatoid arthritis.
  • Osteoarthritis.
  • Plantar fasciitis.
  • Neuropathy.
  • Pelvic girdle pain in pregnancy.
  • Chronic anterior pelvic ring instability.

Vascular:

  • Vascular disease.
  • Claudication.
  • Deep vein thrombosis (DVT).

Neoplastic:

  • Tumour.
  • Pathological fracture.
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7
Q

List the investigations for antalgic gait. (LO1)

A

Depends on the suspected underlying issue and will therefore be subject to the history and examination.

  • X-rays.
  • MRI.
  • CT scan.
  • Ultrasound.
  • Lab tests (e.g. blood or urine samples) - may be taken to help diagnose viral or bacterial infections. In children, lab tests may help identify juvenile rheumatoid arthritis.
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8
Q

Describe the gait pattern in toddlers and young children. (LO1)

A
  • Immature gait pattern.
  • Characterised by broad-based, increased flexion of the hips and knees.
  • Arms beside the body with the elbow extended.
  • Also cannot increase the size of their steps and so increase the pace of their steps to move faster - due to lack of neuromuscular maturity.
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9
Q

List the potential causes of limping in children. (LO1)

A
  • Transient synovitis - usually in the hip secondary to viral infection.
  • Septic arthritis - aspirate to eliminate this option if unclear.
  • Juvenile rheumatoid arthritis.
  • Cerebral palsy.
  • Muscular dystrophy.
  • Developmental dysplasia of the hip.
  • Osteoid sarcoma.
  • Leukaemia.
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10
Q

Describe juvenile rheumatoid arthritis as a cause of limping in children. (LO1)

A
  • Mild and insidious pain in the legs at the start of walking.
  • More common in girls.
  • Knees and ankles most commonly affected.
  • Presentation: swelling, warmth, decreased range of movement.
  • Investigations: WBC, ESR, RF, ANA. These may be normal and should not rule out diagnosis if they are.
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11
Q

When do most children start walking? (LO1)

A
  • First steps at around 12 months.
  • Walking without assistance at around 18 months.

Delay in walking may indicate a neurological disorder.

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12
Q

What is cerebral palsy? (LO1)

A
  • Neurological disorder.

- Leads to claudication when walking, which may go unnoticed before the child’s first steps.

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13
Q

What is muscular dystrophy and how does it differ from cerebral palsy? (LO1)

A

Delay in the beginning of walking accompanied by:

  • Repeated stumbling.
  • Frequent falls.
  • Difficulty climbing stairs due to weakness of muscles proximal to the root of the limb - gluteus maximus, medius and quadriceps.
  • The calf exhibits false hypertrophy and a positive Gower’s sign.
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14
Q

What is Gower’s sign? (LO1)

A

The child is placed in prone position and asked to get up. If they seem to be “climbing over themself”, this is a positive Gower’s sign.

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15
Q

Describe the investigations and prognosis of muscular dystrophy. (LO1)

A
  • Serum CPK - may be 200-300 times the normal level.
  • In general, the patient is taken to the doctor at around 3-6 years of age.
  • May be a positive family history where boys are almost exclusively affected, as it is X-linked recessive.
  • Disease is progressive and evolves slowly.
  • Patients usually die in their 20s/30s from respiratory failure or cardiac arrest.
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16
Q

What are two neoplastic disorders that can cause limping gait in children? (LO1)

A

Osteoid osteoma:

  • > 5 year olds.
  • Claudication pain - mainly at night.
  • May pass undetected on radiographs.
  • Unremarkable clinical examination.
  • Usually no pain on palpation.
  • Significant improvement with aspirin - may increase suspicion.
  • Scintigraphy - highly sensitive in aiding diagnosis.
  • Diagnosis is a challenge, especially, at the start of walking age.

Leukaemia:

  • 2-5 year olds.
  • Claudication pain - even in their first steps.
  • Bone pain, fever and lethargy - similar to arthritis and osteomyelitis.
  • Normal x-ray.
  • Scintigraphy may be unsuccessful.
  • Lab tests at initial stage can also create doubts.
  • Non-specific elevation of ESR and peripheral leukocyte count.
  • Refer to haematologist for bone marrow evaluation.
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17
Q

List the types of abnormal gait. (LO2)

A
  • Antalgic.
  • Short leg.
  • Trendelenburg - weak hip adductors.
  • Stiff knee.
  • Spastic.
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18
Q

Which differentials can short leg gait indicate? (LO2)

A
  • Slipped upper femoral epiphysis (SUFE).
  • Proximal focal femoral deficiency (PFFD).
  • Developmental dysplasia of the hip (DDH).
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19
Q

What is the surgical sieve? (LO2)

A

A surgical sieve is an approach to differential diagnosis that encourages you to consider various types of pathologies systematically.

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20
Q

What is the surgical sieve mnemonic for musculoskeletal deformities? (LO2)

A

VITAMIN CDEF:

  • Vascular.
  • Infective/inflammatory.
  • Trauma.
  • Autoimmune.
  • Metabolic.
  • Iatrogenic/idiopathic.
  • Neoplastic.
  • Congenital.
  • Developmental/degenerative.
  • Endocrine.
  • Functional.
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21
Q

Which of the broad categories of the surgical sieve of musculoskeletal deformities are relevant in children? (LO2)

A
  • Vascular.
  • Infective/inflammatory.
  • Trauma.
  • Autoimmune.
  • Neoplastic.
  • Congenital.
  • Developmental.
  • Functional.
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22
Q

For a limping child, what do we want to know about the history of the presenting complaint? (LO2)

A
  • Acute/chronic?
  • SOCRATES.
  • Trauma.
  • Systemic symptoms - i.e., fever, malaise, anorexia.
  • Joint swelling (NOT HIP).
  • Any previous episodes.
  • Recent infections.
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23
Q

For a limping child, what do we want to know about the past medical history? (LO2)

A

Perinatal history:

  • DDH risk?
  • Birth complications.
  • Special care baby unit (SCBU).

Developmental:
- Milestones - especially gross motor, e.g., walking.

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24
Q

For a limping child, what do we want to know about the family history? (LO2)

A
  • DDH.
  • Inflammatory arthritis.
  • Autoimmune conditions.
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25
Q

For a limping child, what do we want to know about the social history? (LO2)

A
  • Other family members at home.
  • Other carers.
  • Safeguarding concerns.
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26
Q

Describe what you are looking for in a general examination of a limping child. (LO2)

A
  • Well or unwell?
  • Comfortable at rest?
  • Temperature.
  • Pulse.
  • Rashes.
  • Bruises/bites/burns.
  • ENT.
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27
Q

Describe what you are looking for in the LOOK part of a joint examination of a limping child. (LO2)

A
  • Posture of the limb.
  • Fixed flexion deformities.
  • External signs of injury.
  • Swollen joints.
  • Limb length discrepancy.
  • Gait.
  • Erythema.
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28
Q

Describe what you are looking for in the FEEL part of a joint examination of a limping child. (LO2)

A
  • Tenderness.
  • Joint effusion.
  • Muscle tone.
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29
Q

Describe what you are looking for in the MOVE part of a joint examination of a limping child. (LO2)

A
  • Active and passive range of motion.

- Neurological/developmental examination.

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30
Q

Describe the investigation for a limping child. (LO2)

A

Blood tests:

  • FBC - raised WCC for infections.
  • Inflammatory markers - CRP, ESR, raised in infection, inflammation.
  • Autoimmune markers.
  • Blood cultures.

Imaging:

  • Plain radiographs - fractures and dislocations _ bony pathology.
  • Ultrasound - effusions.
  • MRI - bony and soft tissue detail, difficult in <5 year olds as they cannot sit still.
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31
Q

At what ages are the common causes of limp present? (LO2)

A
  • Infection/transient synovitis can occur at ANY AGE.
  • DDH - toddlers - 2-3 years old.
  • Perthes - 4-9 years of age.
  • SUFE - 9-12 years of age.
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32
Q

Describe transient synovitis as a cause of limp in children. (LO2)

A
  • Involves a preceding viral illness.
  • 70% boys.
  • 3-10 years old.
  • Milder symptoms.
  • Bloods - normal to mildly increased inflammatory markers.
  • Normal imaging.
  • No treatment required, recovers spontaneously.
  • Can sometimes prescribe analgesia, e.g., NSAIDs.
  • Main DDx: septic arthritis - MUST RULE OUT.
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33
Q

Describe osteomyelitis as a cause of limp in children. (LO2)

A

Infection within the bone:

  • History of trauma.
  • Range of motion usually less affected.
  • Localised tenderness.

Surgery not usually indicated:

  • Subperiosteal abscess.
  • Intraosseous collection.
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34
Q

Describe septic arthritis as a cause of limp in children. (LO2)

A
  • Infection within the joint space.
  • Range of motion reduced.
  • Effusion.
  • Erythema.
  • Bacterial products and inflammatory mediators destroy cartilage.
  • Washout required urgently.
  • Might have a preceding infection elsewhere.
  • FEVER, UNWELL.
  • Most commonly Staph aureus and Strep.
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35
Q

List the essential investigations for bony infection (limp in children). (LO2)

A

Bloods:

  • CRP.
  • ESR.
  • White cell count.
  • Cultures.

Plain film radiograph:
- X-ray.

Treat with NSAIDs if no contraindications.

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36
Q

What are the indications for surgery in a child with osteomyelitis? (LO2)

A
  • Subperiosteal abscess.

- Large interosseous collection - PVL Staph.

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37
Q

What is DDH? (LO2)

A
  • Developmental dysplasia of the hip.
  • 1/1000 incidence.
  • Spectrum: dysplasia > subluxation > dislocation > instability.
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38
Q

List the risk factors for DDH. (LO2)

A
  • Female.
  • First born.
  • Breech.
  • 1st degree relative family history - parents, siblings, etc.
  • Oligohydramnios - low amniotic fluid during pregnancy.
  • Packing disorders, e.g., torticollis (abnormal muscles of the neck meaning head tilts downwards), metatarsus adductus (metatarsal bones turned inwards towards the body).
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39
Q

What are the two main tests for DDH? (LO2)

A

Barlow’s test:

  • Test of instability.
  • Dislocate the hip from the acetabulum.

Ortolani’s test:

  • Reduce the dislocated hip.
  • Clunk vs. click.

These are performed during neonatal examination. If these are positive or if risk factors present, then ultrasound of the hip at 6-8 weeks.

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40
Q

List the other examinations for DDH. (LO2)

A
  • Allis test - skinfold symmetry.
  • Galeazzi test - leg length discrepancy.
  • Espy abduction of the flexed hip.
  • Gait abnormalities.
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41
Q

Describe the presentation of DDH. (LO2)

A
  • Painless limp (if walking).
  • Leg length discrepancy.

On examination:

  • Restricted range of motion - especially abduction of flexed hip.
  • Leg length discrepancy.
  • Asymmetric skin creases.
  • Abnormal gait.
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42
Q

What is the treatment for DDH? (LO2)

A

Usually determined by age. In order of increasing complexity:

  1. Pavlik harness.
  2. Closed reduction (under general anaesthesia).
  3. Open reduction (under general anaesthesia).
  4. Open reduction with femoral/pelvic osteotomies (under general anaesthetic).
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43
Q

What is Perthes disease? (LO2)

A
  • Idiopathic avascular necrosis of the femoral head.
  • 3/100,000
  • 4-9 year olds (older children have worse prognosis).
  • Males 6:1 females.
  • Females have worse prognosis.
  • Typically, skinny, hyperactive children.
  • Obesity = worse prognosis.
  • 25% bilateral.
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44
Q

List the potential causes for Perthes disease. (LO2)

A
  • Clotting disorder.
  • Passive smoking.
  • Genetic.
  • Environmental.
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45
Q

List the signs of Perthes disease. (LO2)

A
  • Stiff hip - particularly abduction.
  • Pain.
  • Limp.
  • Leg length discrepancy.
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46
Q

What are the four stages of Perthes disease? (LO2)

A
  1. Initial/sclerotic.
  2. Fragmentation.
  3. Healing.
  4. Remodelling.

Classified using the Herring classification.

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47
Q

Describe the management of Perthes disease. (LO2)

A

Main principle is hip containment:

  • Try to keep ball and socket together to keep them congruent.
  • Less congruent the joint, greater the chances of OA later in life.

Methods:

  • Physio for range of motion increase.
  • Brace/plasters.
  • Wheelchair?
  • Bisphosphonates.
  • Surgical:
    1. Femoral osteotomy.
    2. Pelvic osteotomy.
    3. Hip distraction.
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48
Q

What is SUFE? (LO2)

A
  • Slipped upper femoral epiphysis.
  • Femoral head is left POSTERIOR AND INFERIOR.
  • Atraumatic.
  • Usually in OBESE male children.
  • 25% bilateral.
  • Endocrine association - hypothyroid, hypopituitary, CRF (chronic renal failure).
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49
Q

List the symptoms of SUFE. (LO2)

A

Pain:

  • Activity-related.
  • Hip.
  • Could be thigh or knee - always examine the hip of a child with knee pain.

Limp:

  • Antalgic.
  • Externally rotated hip.
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50
Q

Describe the findings on an x-ray of a SUFE. (LO2)

A

MUST be frog leg x-ray of the pelvis.

  • Physeal widening.
  • Trethowan’s sign.
  • Reduced epiphyseal hypertrophic zone.
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51
Q

By which three properties are SUFEs classed? (LO2)

A
  • Temporal (onset).
  • Stability.
  • Severity of slip.
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52
Q

What are the two classes of SUFEs according to the onset? (LO2)

A
  • Acute (less than 3 weeks) - higher rate of avascular necrosis.
  • Chronic.
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53
Q

What are the two classes of SUFEs according to the stability? (LO2)

A
  • Stable - weight-bearing.

- Unstable - non-weight bearing - 50% have avascular necrosis.

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54
Q

What are the three classes of SUFEs according to the severity of the slip? (LO2)

A
  • Mild.
  • Moderate.
  • Severe.

Worse deformity = worse function later in life.

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55
Q

Describe the management for SUFE. (LO2)

A
  • Pin in situ for mild/moderate.
  • DON’T ATTEMPT REDUCTION - risk of avascular necrosis.
  • Femoral osteotomy to re-shape the femur - early or late.
  • If severe - open reduction and osteotomy - avascular necrosis risk.
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56
Q

Describe the flowchart used in diagnosing limp in children. (LO2)

A
  1. Pain?
    - No - DDH, LLD, hemiplegia.
    - Yes - question 2.
  2. Acute?
    - No - Perthes, SUFE, tumour, JIA (juvenile idiopathic arthritis).
    - Yes - question 3.
  3. Trauma?
    - No - question 4.
    - Yes - Injury, fracture.
  4. Systemic upset?
    - No - Perthes, SUFE, tumour, JIA (juvenile idiopathic arthritis).
    - Yes - Infection, irritable hip, JIA, acute lymphoblastic leukaemia.
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57
Q

Which muscles are involved in the heel-strike part of gait? (LO2)

A

The foot must be dorsiflexed so:

  • Tibialis anterior.
  • Gluteus maximus and posterior capsule.
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58
Q

Which muscle is involved in the loading response (foot flat after heel-strike)? (LO2)

A

Quadriceps femoris.

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59
Q

Which muscle are involved in the mid-stance (foot flat after heel-strike and other foot leaves floor)? (LO2)

A
  • Triceps surae (gastrocnemius x2 and soleus).

- This moves into the terminal stance/heel off which involves plantarflexion.

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60
Q

Which muscles are involved in the toe-off part of gait? (LO2)

A
  • Deep plantar flexors.
  • Flexors of the toes.
  • Intrinsic foot muscles.
  • Rectus femoris.
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61
Q

Which muscles are involed in the initial and mid-swing part of gait? (LO2)

A
  • Contralateral abductors of the hip.
  • Iliopsoas.
  • Rectus femoris.
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62
Q

Which muscles are involved in the terminal swing part of gait (foot about to be planted but still swinging)? (LO2)

A
  • Quadriceps femoris.
  • Tibialis anterior.
  • Hamstrings.
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63
Q

What are the pre-requisites for gait? (LO2)

A
  • Stability in stance.
  • Sufficient foot clearance in swing.
  • Appropriate pre-positioning of the foot in swing.
  • Adequate step length.
  • Energy conservation.
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64
Q

Which anatomical structures can affect gait? (LO2)

A
  • Joints, e.g., arthritis.
  • Bones, e.g., deformities.
  • Muscles, e.g., muscular dystrophy and spasticity.
  • Nerves, e.g., trauma.
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65
Q

List the types of abnormal gait (Mnemonic: STRAWS). (LO2)

A
  • Short leg.
  • Trendelenburg.
  • Rigid.
  • Antalgic.
  • Weak.
  • Supratentorial.
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66
Q

List the potential causes of short leg gait. (LO2)

A
  • Bowing at the femur - valgus deformity.
  • Leg length discrepancy.
  • Shorter left femur - diagnosis: Proximal focal femoral deficiency (PFFD).
  • Shorter femoral neck - diagnosis: Perthes.
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67
Q

Describe how we can identify short leg gait. (LO2)

A
  • Head and shoulder drop as the patient steps onto short limb (head bobs in sagittal plain).
  • Pelvis drops on affected side during heel strike.
  • Vaulting gait - elevate pelvis and proximal femur of stance leg, allows for longer leg to swing through.
  • Flexion of the knee, equinus ankle of longer leg (limited dorsiflexion).
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68
Q

Describe how we can identify Trendelenburg gait. (LO2)

A
  • Excessive lateral trunk flexion.
  • Weight shifting over the stance leg.
  • Positive Trendelenburg test.
  • Possibly due to hemiarthroplasty.

Weakness of abductor mechanism:

  • Joint: subluxed, dislocated hip.
  • Bone - shortening of femoral neck.
  • Muscle - abductor weakness.
  • Pain.
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69
Q

Describe how we can identify rigid gait. What would you see if the abnormality causing this gait was in different joints of the lower limb? (LO2)

A

Hip abnormality:

  • Head and torso sways from the front to back in sagittal plan while walking.
  • Decreased hip flexion on swing phase and lumbar motion increases.

Knee abnormality:

  • Hip circumducts.
  • Little flexion/extension through stance.

Ankle abnormality:

  • May turn foot our to use subtalar joint (STJ).
  • Limitation flexion/extension in sagittal plan.
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70
Q

Describe how we can identify antalgic gait. (LO2)

A
  • Shortened stance phase.
  • Avoids weightbearing on that side.
  • Avoids heel-strike.

What happens at the hip?:
- Lurches over the painful side to reduce lever arm and hence joint reaction force (JRF).

What happens in the knee?:
- Held slightly flexed.

This is one person and these are the features you would see on the patient simultaneously.

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71
Q

What is joint reaction force (hip)? (LO2)

A
  • Joint reaction force is defined as the force generated within a joint in response to forces acting on the joint.
  • In the hip, it is the result of the need to balance the moment arms of the body weight and abductor tension. You work to lower the joint reaction force when in pain.
    (- A moment arm is simply the length between a joint axis and the line of force acting on that joint.)
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72
Q

How does the body work to lower the JRF at the hip? (LO2)

A
  • The abductors work to take some of the pressure off your joints.
  • The same can be done with a stick.
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73
Q

What happens to the knee joint when you put your full body weight on it? (LO2)

A

By doing this, you force the knee into hyperextension.

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74
Q

Describe how we can identify weak gait. What would you see if the abnormality causing this gait was in different joints of the lower limb? (LO2)

A

Hip abnormality:
- Trendelenburg.

Knee abnormality:

  • Weak quadriceps.
  • Back-knee.

Ankle abnormality:

  • High-stepping gait (usually due to foot drop/common peroneal nerve injury).
  • Hip/knee flexed excessively to lift foot.
  • Foot slap on initial contact.
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75
Q

Describe how we could identify spastic gait. (LO2)

A
  • No heel-strike on the right foot.

- Right leg adducted and internally rotated.

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76
Q

What are hemiplegia and diplegia? (LO2)

A
  • Brain injury resulting in varying degrees of weakness, (stiffness) spasticity and lack of control.
  • Hemiplegia = affecting one side of the body.
  • Diplegia = affecting both sides of the body.

Diplegia can be asymmetrical so if one side is more affected than the other, it can look like hemiplegia (only one side affected).

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77
Q

What are the two causes of supratentorial (neuromuscular) gait? (LO2)

A
  • Spastic hemiplegia.

- Spastic diplegia.

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78
Q

Describe how we can identify supratentorial gait caused by spastic HEMIplegia. (LO2)

A
  • Unilateral loss of heel strike.
  • Knee held flexed.
  • Nil movement of arm in swing.
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79
Q

What are the four types of gait which can be seen in spastic DIplegia? Describe them. (LO2)

A
  1. Equinus gait - nil heel strike in rocker phases.
  2. Jump gait - ankle equinus (lack of dorsiflexion), knee flexion.
  3. Crouch gait - ankle/knee + hip flexion.
  4. Scissoring gait.
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80
Q

Describe the management of abnormal gait. (LO2)

A
  • History.
  • Examination.
  • Investigations.
  • Treat the underlying cause - weight reduction, physio, orthotics and aids, e.g., walking sticks.
  • Surgery.
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81
Q

What surgical interventions can be taken to improve abnormal gait? (LO2)

A
  • Joint replacement.
  • Re-shape bone (osteotomy).
  • Lengthen/divide/transfer muscles - will weaken and cannot make weak muscles stronger.
82
Q

Describe the epidemiology of child abuse. (LO3)

A
  • Around 30% of children suffer abuse.

- It causes long-term emotional harm.

83
Q

List some injuries suggesting non-accidental cause. (LO3)

A
  • Injuries in non-ambulant babies - abuse more likely in younger children.
  • Bruising - face, ear, head, back, buttocks, soft tissue areas.
  • Slap, pinch, bite marks.
  • Burns, brands, cigarette marks.
  • Fractures in infants - especially ribs.
  • Subdural bleeding, especially with encephalopathy and retinal haemorrhage.
  • Peri-oral - injuries to the mouth.
84
Q

List some general factors associated with abuse. (LO3)

A
  • Domestic violence.
  • Parental substance abuse.
  • Parental mental illness.
85
Q

List some social factors associated with abuse. (LO3)

A
  • Poverty.
  • Young parents.
  • Social isolation.
  • 3 children or more under 5 years.
86
Q

List some factors associated with abuse relating to the parents. (LO3)

A
  • Learning difficulties.
  • Bad experiences of parenting.
  • Personal history of abuse.
87
Q

List some factors associated with abuse relating to the child in question. (LO3)

A
  • Disability.
  • Preterm delivery.
  • Multiple pregnancy.
88
Q

List the red flags for abuse (NAIs) in children presenting with fractures. (LO3)

A
  • Multiple fractures.
  • Different ages.
  • Include rib fractures.
  • Age less than a year.
  • Absence of a credible history.
  • Metaphyseal.
  • Younger child.
89
Q

List some common sites of accidental fractures in children. (LO3)

A
  • Supracondylar.
  • Toddler fractures.
  • Wrist.
90
Q

List the three main categories of causes of fractures in children. (LO3)

A
  • Accident.
  • Neglect.
  • Abuse.
91
Q

How do we spot child abuse from the history? (LO3)

A
  • Delay in presentation.
  • Story not credible.
  • Changeable story.
92
Q

How do we spot child abuse from the examination of the injury? (LO3)

A
  • Injuries don’t fit the story.

- Injuries not compatible with development.

93
Q

Which features of a general examination of a child can tell us about child abuse? (LO3)

A
  • Thriving or not - height and weight?
  • Well cared for or not - clean, dressed appropriately?
  • Is the child secure and settled with the parent, or fearful?
  • Development - appropriate or not?
  • Attachment - does the child seek security from the parent?
94
Q

How is child abuse managed? (LO3)

A
  • Good record keeping.
  • Pictures or photographs.
  • Share concerns with a colleague or supervisor.
  • Report the case to children’s services.
95
Q

What are podiatrists? (LO4)

A

Healthcare professionals who have been trained to diagnose and treat abnormal conditions of the feet and lower limbs.

96
Q

What do podiatrists do? (LO4)

A

Treat abnormal conditions of the feet AND lower limbs.

  • Prevent and correct deformity.
  • Prevent skin lesions.
  • Keep people mobile.
  • Relieve pain.
  • Treat infections.
  • Give advice on care of your feet and what type of shoes to wear.
  • Give advice on orthotics to improve the mechanics of deformed feet.
97
Q

Which part of the body do podiatrists focus on? (LO4)

A

Feet AND lower limbs.

98
Q

List the day-to-day foot problems that podiatrists can help with. (LO4)

A
  • Toenail problems: thickened toenails, fungal nail infections, ingrown toenails.
  • Corns and calluses.
  • Verrucas.
  • Athlete’s foot.
  • Smelly feet.
  • Dry and cracked heels.
  • Flat feet.
  • Bunions.
  • Heel pain.
  • Ageing feet.
  • Blisters.
  • Gout.
  • Sports injuries.
99
Q

What is another word for a podiatrist? (LO4)

A

Chiropodist - although this is less frequently used now.

100
Q

What is a biomechanics assessment? When is it required? (LO4)

A
  • An investigation into your lower limb function, looking very closely for any abnormalities that may cause pain or discomfort.
  • People have an assessment done when the abnormalities in their feet start to impact their day-to-day lives and activities.
101
Q

What is meant by biomechanics when referring to podiatry? (LO4)

A

Refers to the way the bones, muscles and joints of your feet and lower limb interact and move. Specifically looks at:

  • Pronation - how impact is absorbed.
  • Supination - how you are propelled.
102
Q

Describe pronation of the foot in gait. (LO4)

A

Absorption:

  • The movement of your foot as the weight is transferred from the outside of the heel to the inside of the forefoot.
  • This helps the foot adapt to different surfaces and cope with the impact when you put your foot down.
  • A degree of pronation is required for walking and running.
  • Too much, or not enough, leads to strain, injury and eventually chronic pain.
103
Q

Describe supination of the foot in gait. (LO4)

A

Propulsion:

  • When the front of your foot pushes forward to lift your heel and move the weight forward to the front of your foot and your toes.
  • Supination happens after your foot has absorbed the impact of putting your foot down.
  • This is what propels you in the direction you want to travel.
  • Too much, or not enough, of supination can lead to injury and pain.
104
Q

List the basic aspects of a biomechanics assessment (by a podiatrist). (LO4)

A
  1. Take a fully medical history + basic tests (e.g. neurovascular assessment).
  2. Assess balance deficits + postural control and gait.
  3. Discuss concerns, make diagnosis and treatment plan.
105
Q

How does a podiatrist assess balance deficits, postural control and gait as part of a biomechanical assessment? (LO4)

A
  1. Simple hallway assessment.
  2. Record simple hallway assessment to review in future.
  3. Treadmill.
  4. Pressure-mapping.
106
Q

What does a simple hallway assessment entail as part of a biomechanical assessment by a podiatrist? (LO4)

A
  1. Have the patient walk up and down to assess their gait.
  2. Gives a view of both the front and the back of the person.

However, clothing may change gait or make it difficult to assess.

107
Q

Why are results from the simple hallway assessment recorded by a podiatrist? (LO4)

A
  • Allows you to assess the patient’s gait from multiple angles.
  • Allows documentation of the patient’s gait for assessing changes to gait over time, monitoring responses to treatment.
  • Allows for a general review.
108
Q

Why is the treadmill useful in a biomechanical assessment by a podiatrist? (LO4)

A

Makes it easier to take videos and pictures from different angles.

109
Q

How is pressure-mapping useful in a biomechanical assessment by a podiatrist? (LO4)

A
  • Allows you to see areas of high and low pressure during the stance phase of gait (where most pathology occurs).
  • Very useful for people with peripheral neuropathy as they cannot give you feedback on where they feel pressure.
  • Can aid the development of treatments, e.g., orthotics.
  • Helps you to assess treatment goals.
  • Can provide information on weight-bearing distribution.
110
Q

What is the main aim of a biomechanics assessment? (LO4)

A

To restore as much symmetry and alignment as possible. Can do this using orthotics:

  • E.g. tailor-made insoles, padding and arch supports to relieve arch or heel pain.
  • Orthotics are put into shoes to realign foot, take pressure off vulnerable areas of the foot and/or to make shoes more comfortable.
111
Q

Why do we perform a gait analysis? (LO4)

A
  • Helps to diagnose biomechanical imbalances.
  • To help perform a thorough biomechanical examination.
  • To help determine why pressure ulcers form.
    Assessing gait and analysing motion gives insight into how pathology occurs.
112
Q

What is the difference between in/eversion and pro/supination? (LO4)

A

Inversion is often used interchangeably with supination, as is eversion with pronation, but they aren’t exactly the same:

  • Inversion/eversion are frontal plane motions of the ankle.
  • Pronation/supination are triplanar motions of the foot/ankle complex.
113
Q

Define inversion. (LO4)

A
  • As the calcaneus/heel moves in the direction so that the bottom of your foot faces inwards.
  • When this happens in excess, an inversion sprain and/or an injury somewhere up the chain is likely to occur.
  • Occurs at the hindfoot (heel).
114
Q

Define eversion. (LO4)

A
  • As the calcaneus/heel moves in the direction so that the bottom of your foot faces outwards.
  • When this happens in excess, an injury may occur with excessive movement and/or stress in this direction.
115
Q

Define supination. (LO4)

A

Combination of:

  • Inversion of the hindfoot.
  • ADduction of the forefoot.
  • Plantarflexion of the talocrural (ankle) regions.
116
Q

Define pronation. (LO4)

A

Combination of:

  • Eversion of the hindfoot.
  • ABduction of the forefoot.
  • Dorsiflexion of the talocrural (ankle) regions.
117
Q

List the clinical features of muscle disorders. (LO5)

A
  • Weakness: proximal vs symmetrical vs persistent.
  • Weakness>wasting.
  • Normal sensation.
  • Normal tendon reflexes (or decreased in areas of prominent weakness).
  • May also present with myotonia, rhabdomyolysis, cardiomyopathy or contractures.
118
Q

List the investigations for muscle disorders. (LO5)

A
  • EMG.
  • Serum CK (high).
  • FBC.
  • U+Es.
  • Endocrine tests, e.g., thyroid function - thyroid disease can cause proximal myopathy.
  • Muscle biopsy.
  • Genetic testing.
  • Antibody testing.
119
Q

Which antibodies are positive in connective tissue disease? (LO5)

A
  • ANA.
  • RF.
  • Anti-dsDNA.
  • Anti-Ro.
  • Anti-La.
  • Anti-Scl-70.
120
Q

Which antibody is polymyositis positive for? (LO5)

A

Anti-Jo1.

121
Q

Which antibody is dermatomyositis positive for? (LO5)

A

Anti-Mi2.

122
Q

What are the two types of causes of myopathy? (LO5)

A
  • Acquired.

- Inherited.

123
Q

List the types of acquired myopathy. (LO5)

A
  • Inflammatory - polymyositis, dermatomyositis, inclusion body myositis.
  • Endocrine - thyroid, pituitary, parathyroid, adrenal, hypokalaemia, hypo/hypercalcaemia.
  • Alcohol.
  • Infectious, e.g., HIV.
  • Paraneoplastic.
124
Q

List the patterns of inheritance used when myopathies are passed on. (LO5)

A

Mutations in NUCLEAR genes coding for constituent proteins associated with muscle membranes.

  • X-linked.
  • Autosomal dominant.
  • Autosomal recessive.
  • Mitochondrial - maternal inheritance, multi-system involvement.
125
Q

What are the two categories of inherited myopathies? (LO5)

A
  • Non-dystrophic myopathy.

- Muscular dystrophy.

126
Q

List the types of non-dystrophic myopathy. (LO5)

A
  • Congenital.
  • Mitochondrial.
  • Familial periodic paralysis.
  • Metabolic, e.g., phosphorylase deficiency (McArdle’s disease), acid maltase deficiency (Pompe’s disease).
127
Q

List the types of muscular dystrophy. (LO5)

A
  • Becker.
  • Duchenne.
  • Facioscapulohumeral.
  • Myotonic.
  • Emery dreifuss.
  • Limb-girdle.
  • Oculopharyngeal.
  • Congenital.
128
Q

Describe muscular dystrophies and the basis of their classification. (LO5)

A

Genetically determined diseases characterised by:
- Progressive degenerative change in muscle fibres.
- Muscle weakness.
Classified based on:
- Clinical distribution of weakness.
- Pattern of inheritance.
- Molecular genetics.

129
Q

List the X-linked muscular dystrophies. (LO5)

A
  • Duchenne and Becker.

- Emery Dreifuss.

130
Q

List the autosomal dominant muscular dystrophies. (LO5)

A
  • Facioscapulohumeral (FSHD).
  • Myotonic dystrophy.
  • Scapuloperineal.
  • Oculopharyngeal.
  • Limb girdle 1 (LGMD1).
  • Distal.
131
Q

List the autosomal recessive muscular dystrophies. (LO5)

A
  • Limb girdle 2 (LGMD2).
  • Scapulohumeral.
  • Distal.
132
Q

Describe the clinical and genetic features of Duchenne muscular dystrophy. (LO5)

A
  • X-linked recessive.
  • Frameshift mutation in the DYSTROPHIN gene.
  • Onset 3-5 years.
  • More common in male children.
  • Progressive muscle weakness, usually proximal.
  • Unable to stand without using hands for support, walking difficulty, cannot climb stairs.
  • Waddling gait.
  • Gower’s sign - uses hands to stand up from sitting.
133
Q

Describe the clinical features of Duchenne muscular dystrophy. (LO5)

A
  • Muscle pseudohypertrophy - especially calf due to collagen and adipose replacement of muscle tissue.
  • MSK - scoliosis + contractures.
  • Other - DILATED CARDIOMYOPATHY, low IQ.
  • Premature death - 15-25 years old, cardiac/respiratory failure.
134
Q

What is the function of the dystrophin gene? (LO5)

A
  • Codes for dystrophin protein.
  • Stabilises the membrane during contraction and relaxation.
  • Part of the link between intracellular cytoskeleton and extracellular matrix.
  • Enables muscle fibres to differentiate into fast glycolic/fast twitch fibres.
  • Organisation of post-synaptic membrane and AChRs.
135
Q

Describe the clinical and genetic features of Becker muscular dystrophy. (LO5)

A
  • X-linked recessive.
  • In-frame dystrophin mutation.
  • MILD FORM OF DUCHENNE MUSCULAR DYSTROPHY.
  • Boys >7 years old (avg. 11 years old).
  • Slowly progressive, weakness tend to be proximal - especially quads and pelvic + arms.
  • Toe-walking.
  • Gower’s sign - weakness in proximal hip muscles.
  • Severity is correlated with dystrophin levels.
136
Q

Describe the clinical features of Becker muscular dystrophy. (LO5)

A
  • Calf hypertrophy.

Systemic features:

  • Cardiomyopathy.
  • Respiratory muscle involvement.
  • Scoliosis.
  • Mild learning difficulty.
137
Q

Describe muscle biopsy results of DMD and BMD as opposed to normal results. (LO5)

A
  • Normal: dystrophin stains around rim of muscle fibres.
  • Duchenne: dystrophin ring is absent.
  • Becker: dystrophin ring is visible but less stained.
138
Q

Describe the features of facioscapulohumeral dystrophy (FSHD). (LO5)

A
  • Type 1 and type 2.

- Autosomal dominant but 1/3 is a de novo mutation.

139
Q

Describe the clinical features of facioscapulohumeral dystrophy (FSHD). (LO5)

A

Weakness:

  • Face - ptosis, cannot whistle.
  • Upper extremity.
  • Scapular winging.
  • Humeral.
  • Peroneal muscles (foot drop).

Other:

  • Cardiac.
  • Hearing.
  • Epilepsy.
  • Learning difficulty.
140
Q

Describe the features of myotonic dystrophy. (LO5)

A
  • Autosomal dominant.
  • Most common ADULT muscular dystrophy.
  • Slow progressing multi-system disease.
  • Two types: DM1 (Steiner’s disease) and DM2 (proximal myotonic myopathy PROMM).
141
Q

List the clinical features of myotonic dystrophy. (LO5)

A
  • Frontal balding.
  • Cataracts.
  • Myopathic facies - facial weakness.
  • Muscle wasting/weakness.
  • Myotonia.
  • Cardiac conduction defects.
  • Cardiomyopathy.
  • Sleep apnoea.
  • Hypersomnolence.
  • Gynaecomastia.
  • Diabetes.
  • Hypogonadism.
142
Q

Describe type 1 myotonic dystrophy (DM1). (LO5)

A
  • Anticipatory, i.e., it gets worse with every generation.

- Affects the DMPK gene on chromosome 19 (Ch19).

143
Q

Describe type 2 myotonic dystrophy (DM2). (LO5)

A
  • Milder than DM1.
  • CNBP gene mutation.
  • Minimal/no anticipation.
144
Q

What is ataxia? (LO5)

A
  • Lack of coordination.

- 2 types of ataxic gait: cerebellar and sensory.

145
Q

Describe cerebellar ataxic gait. (LO5)

A

Wide-based gait, associated with intention tremor/limb ataxia.

146
Q

Describe sensory ataxic gait. (LO5)

A

Unsteady, high stepping. Worse in the dark because they can’t feel if their foot has touched the ground so will often stomp.

147
Q

List the two types of causes of cerebellar ataxias. (LO5)

A
  • Acquired.

- Hereditary.

148
Q

List the types of acquired cerebellar ataxias. (LO5)

A
  • Vascular.
  • Drugs.
  • Infection.
  • Tumours.
  • Hypothyroid.
  • Vitamin E/B12 deficiency.
  • Prion disease.
  • Paraneoplastic.
149
Q

List the types of hereditary cerebellar ataxias. (LO5)

A
  • Autosomal recessive - Friedrich’s ataxia.
  • Autosomal dominant cerebellar ataxia (ADCA).
  • Autosomal dominant episodic ataxia.
  • Mitochondrial.
150
Q

Describe the features of Friedrich’s ataxia. (LO5)

A
  • Commonest inherited ataxia.
  • Autosomal recessive.
  • GAA trinucleotide repeat in X25 gene for frataxin.
  • Onset before 25 years old (avg. 10 years old).
  • Gait and limb ataxia.
  • Pes cavus - high foot arch that does not flatten with weight-bearing.
151
Q

List the clinical features of Friedrich’s ataxia. (LO5)

A
  • Areflexia in lower limb.
  • Pyramidal weakness.
  • Extensor plantar response.
  • Impaired joint position sense.
  • Death in mid-30s.
  • Scoliosis.
  • Diabetes.
  • Neurological variations.
  • HYPERTROPHIC CARDIOMYOPATHY: heart failure, cardiac arrhythmias.
152
Q

Describe the features of autosomal dominant cerebellar ataxias (ADCA). (LO5)

A
  • Adult onset.
  • Complicated classification.
  • 27 subtypes.
  • May show anticipation.
  • Variable features in addition to ataxia: cerebellar features, spasticity, ophthalmoplegia, SCA7 (pigmentary maculopathy) and SCA15 (tremor).
153
Q

What is included in the 27 subtypes of autosomal dominant cerebellar ataxias? (LO5)

A
  • Spino-cerebellar ataxias (SCA) - many types.

- Dentatorubral pallidoluysian atrophy (DRPLA) - ataxia, choreoathetosis, myoclonus and dementia.

154
Q

List the functions of a motor control system. (LO6+7+8)

A

Functions:

  • Posture and balance.
  • Goal-directed movements - e.g. raising a glass to drink from.
  • Communication.
155
Q

What role does the sensory system play in the motor control system? (LO6+7+8)

A
  • Detects changes in the environment.
  • Our motor system can’t react without a sensory system.
  • Degradation of our sensory systems will have an impact on our motor systems.
156
Q

What are the classes of movements (neurologically)? (LO6+7+8)

A
  • Voluntary.
  • Reflexes.
  • Rhythmic motor patterns.
157
Q

Describe voluntary movement. (LO6+7+8)

A
  • Complex actions (reading, writing).
  • Purposeful goal directed.
  • Learned.
158
Q

What are reflexes? (LO6+7+8)

A
  • Involuntary.
  • Rapid.
  • Stereotypes (knee jerk, eye blink).
159
Q

What are rhythmic motor patterns of movement? (LO6+7+8)

A
  • Combines voluntary and reflexive acts (chewing, walking, running, breathing).
  • Initiation and termination is voluntary.
  • Once initiated, repetitive and reflexive.
160
Q

Describe the organisation of the spinal cord. (LO6+7+8)

A
  • Primary sensory afferents (reflexes) enter the dorsal horn and terminate within laminae I, II and VI.
  • Lamina VI receives sensory information from muscles and joints.
  • These afferents synapse with interneurons which travel down to the anterior horn where they meet cell bodies of the specific motor neurones.
  • These cell bodies work medially to supply the muscles of the trunk, and distally to supply the periphery. They are also organised anteriorly and posteriorly.
  • Motor neurones for muscles that flex limbs lie more dorsal.
  • Motor neurones for muscles that extend limbs lie more ventral.
161
Q

What is a motor unit? (LO6+7+8)

A
  • The motor fibre and all the skeletal muscle fibres that it innervates.
  • A single motor neurone will innervate a motor unit (a number of skeletal muscle fibres of the same type).
  • Size-dependent - e.g. if you want fine motor control, you’d have small motor units of fewer skeletal muscle fibres: in fingers, motor units made up of about 6 skeletal muscle fibres.
162
Q

What are Renshaw cells? (LO6+7+8)

A
  • Axons involved in reflex pathways in the spinal cord.
  • Even in simple pathways, we do have some axons (Renshaw cells) that branch back into the spinal cord and synapse with interneurons.
  • These provide that internal feedback and inhibition.
  • This is because we might want to modulate the firing rate of particular neurones, and as such the muscle activity.
163
Q

What is a muscle spindle? (LO6+7+8)

A
  • A structure that lies within the muscle fibre.
  • Detects when a muscle is lengthening (relaxing), as opposed to golgi tendon organs which detect when a muscle is contracting.
  • It doesn’t have any contractability and doesn’t add any force into the muscle.
  • It’s there to monitor the muscle itself.
164
Q

Explain the role of the muscle spindle in a muscle that contracts too much. (LO6+7+8)

A
  • When a muscle stretches, the thin fibres come away from the cross-bridges with the thick fibres.
  • This is when we get a really long muscle that doesn’t have that much force.
  • If it’s pulled too much, and it detaches from the cross-bridges, then we get a rupture/tear in the muscle.
  • The muscle spindle identifies the stretching of the muscle and tries to counteract the excessive stretching.
165
Q

Explain the role of the muscle spindle in a muscle that relaxes too much. (LO6+7+8)

A
  • When a muscle relaxes too much, the muscle gets damaged.
  • The muscle spindle identifies the exact length and communicates this to the nervous system. This also tells the nervous system where exactly the muscle is (proprioception).
  • This occurs using information such as exact length and attachments of the muscle.
166
Q

Which neurones are involved with identifying length and stretch of muscles? (LO6+7+8)

A
  • Group I and Group II afferent axons.

- They also identify the rate of stretch (speed with which it is stretching).

167
Q

Which neurones are involved with modifying muscle stretch, etc.? (LO6+7+8)

A
  • Axons of Aγ-motor neurones.
  • These can change the length of the muscle.
  • We can modify the length of our muscles by stretching, so these neurones can modify the set length information in the muscle spindle.
168
Q

Describe how the myotatic (knee jerk) reflex works neurologically. (LO6+7+8)

A

Hitting the patellar tendon mimics the lengthening of the quads so a signal is sent to the spinal cord to do the opposite and very quickly (to avoid damage).

  1. Sensory afferents (from the muscle spindle of the quads) send signals to the dorsal horn and synapse with the motor neurone of the SAME muscle (quads) in the ventral horn.
  2. The motor neurone contracts the quads and when that happens, the foot moves (knee extends) as a reflex.
  3. As muscles work in pairs, and the body is telling the quads to contract, it also has to tell the associated muscle (hamstrings) to lengthen.

Muscles cannot be turned off, only turned on.

  1. The motor neurone leading to the hamstrings is INHIBITED. This inhibits the action potential and stops the contraction of the hamstrings. This allows contraction of the quads.
169
Q

What is a golgi tendon organ? (LO6+7+8)

A
  • A structure that lies within tendons of muscles.
  • Detects when a muscle is stretching (contracting), as opposed to muscle spindles which detect when a muscle is relaxing.
  • More precisely, it tells us about the FORCE of contraction.
170
Q

How does the golgi tendon organ obtain information about a muscle contracting? (LO6+7+8)

A
  • Tendons have no contractability, only muscles. But as the muscle contracts, the tendon has to lengthen in some way.
  • The spaghetti mesh structure in the tendon straightens out when the muscle contracts.
  • Overcontraction can lead to rupture of the muscle or tendon.
171
Q

What information does the golgi tendon organ relay? (LO6+7+8)

A

Activated by muscle stretch and contraction.

  • Static length of the muscle.
  • Rate of change in length.
  • Force generated during contraction.
  • Exact location of the muscle and therefore, the limb.
172
Q

Describe the sensory innervation of golgi tendon organs. (LO6+7+8)

A
  • Involves group 1b afferents.

- Wrapped around bundles of collagen fibres in the tendon of a muscle.

173
Q

What is the PRIMARY goal of a golgi tendon organ? (LO6+7+8)

A

To prevent damage from overcontraction of a muscle.

174
Q

What is the SECONDARY goal of a golgi tendon organ? (LO6+7+8)

A

To communicate to the spinal cord information about where a muscle or limb is in the body.

175
Q

Explain how the inverse myotatic (golgi tendon) reflex works neurologically. (LO6+7+8)

A

When the muscle becomes too contracted:

  1. Group 1b sensory afferents (from the golgi tendon organs of the quads) send signals to the dorsal horn of the spinal cord.
  2. One branch synapses with the motor neurone of the same muscle that the sensory afferent originated in (quads) and provides inhibitory signals. The quads lengthen.
  3. One branch synapses with a motor neurone innervating the hamstring muscle and provides excitatory signals. The hamstrings contract.
176
Q

Give an example of a withdrawal reflex. (LO6+7+8)

A

If we step on something sharp or if we experience pain of some sort from an external force, our natural response is to withdraw.

177
Q

Example: a person steps on a sharp object with their right foot.

Why is a withdrawal reflex alone not sufficient in this case? (LO6+7+8)

A

If the person were to just withdraw their foot, they would lose their balance and potentially fall:

  • The body must enable the limb to come away from the pain without losing balance.
  • So it has to modulate and change postural control at the same time - this is called the CROSSED EXTENSOR REFLEX.
178
Q

Example: a person steps on a sharp object with their right foot.

Explain how the withdrawal and crossed extensor reflex works neurologically, using this example. (LO6+7+8)

A
  1. C-fibre sensory afferents send pain signals to the spinal cord where there are multiple synapses. All the synapses lead to interneurons and then onto the motor neurones.
  2. Synapse 1: inhibitory effect the quads in the right leg (injured leg).
  3. Synapse 2: excitatory effect on the hamstrings in the right leg (injured leg).
  4. So far, the effect is to pick up the right heel and move it towards the bum. The hamstrings are stimulated to flex at the knee and withdraw.
  5. Synapse 3: excitatory effect on the quads in the left leg.
  6. Synapse 4: inhibitory effect on the hamstrings in the left leg.
  7. These impulses allow the left quads to contract and the left hamstrings to relax. This allows weight to be put on the left leg for balance.
179
Q

Explain how the withdrawal and cross-extensor reflex can work in other parts of the body. (LO6+7+8)

A
  • We might get similar interactions at different levels in the spinal cord, allowing for effects in the trunk, arms, etc. to allow for more balance.
  • E.g. when standing on one leg, you may begin to shake. This is the effect of obvious excitation and inhibition of different muscles.
  • This happens because muscle spindles and golgi tendon organs send so much information to the spinal cord and this is to excite and inhibit various muscles to maintain balance as we go through day-to-day life.
180
Q

What is the central pattern generator (CPG)? (LO6+7+8)

A
  • A pattern for locomotion.
  • Located in the spinal cord.
  • Capable of autonomous signals.
  • Modulated by proprioceptive input.
181
Q

When is the central pattern generator (CPG) useful? (LO6+7+8)

A
  • When we use lots of different reflexes to run in a repetitive motion, such as walking.
  • Once we get started, we should be able to involuntarily continue such activities.
  • There are particular regions for flexor and extensor mechanisms.
182
Q

Which region of the central pattern generator (CPG) controls the flexor muscles? (LO6+7+8)

A
  • The flexor motor neurone pool.

- E.g. swing phase of locomotion.

183
Q

Which region of the central pattern generator (CPG) controls the extensor muscles? (LO6+7+8)

A
  • The extensor motor neurone pool.

- E.g. stance phase of locomotion.

184
Q

The central pattern generator has an internal network between the two pools. How does this work? (LO6+7+8)

A
  • The inhibitory interneuron is the basis for the internal network.
  • It will inhibit the flexors and excite the extensors, and vice versa.
  • As the muscles extend, we get information from the muscle spindle, to tell us that the muscle is extending, into the extensor pool. This tells the flexor muscles to be inhibited.
  • However, within the extensor pool, another signal is sent within its own internal negative feedback system. This continues until the extensor mechanism turns off and allows the flexor mechanism to be turned on.
  • This goes back and forth.
185
Q

Where is the primary motor cortex located? (LO6+7+8)

A
  • Posterior part of the frontal lobe.

- Output through the corticospinal tract.

186
Q

Where is supplementary motor area (SMA) located? (LO6+7+8)

A

Just in front of the motor cortex.

187
Q

How does the homunculus represent the motor cortex? (LO6+7+8)

A
  • It is a graphical representation of the body throughout this motor cortex.
  • The amount of space allocated to a particular part of the body would give an indication to the amount of neurones and space that we have within the motor cortex for that part.
  • Areas with a larger amount would have a larger degree of variability and so fine motor control (e.g. hands, lips, face). Trunk and shoulders would only have gross motor control.
  • The homunculus can be imprinted onto the primary motor cortex with the legs, hip and feet sitting at the centre, to the tongue, etc, sitting at the lateral areas.
188
Q

Which side of the body is controlled by the primary motor cortex? (LO6+7+8)

A

Controls muscles of the opposite side of the body.

189
Q

Which side of the body is controlled by the secondary (supplementary) motor area (SMA)? (LO6+7+8)

A

Can control muscles on both sides of the body.

190
Q

What is the basal ganglia? (LO6+7+8)

A

A group of structures that are deeper than the cerebral hemisphere. They are located in an area sitting above the midbrain. They are involved in correction and memory of movement.

191
Q

List the structures making up the basal ganglia. (LO6+7+8)

A
  • Caudate - split into tail, body and head and wraps around the thalamus.
  • Putamen - sits right through the middle.
  • Globus pallidus - sits in the medial part, behind the putamen (isn’t usually visible in diagrams) - made up multiple nuclei.
  • Substantia nigra - made up of multiple nuclei.
  • Subthalamic nucleus.
192
Q

What is the striatum? (LO6+7+8)

A

A collective term for the caudate and putamen.

193
Q

Describe the subthalamic nucleus (basal ganglia). (LO6+7+8)

A
  • Not an anatomical feature of the basal ganglia.
  • Has such an interaction with the physiology of the basal ganglia, that it is included as a structure.
  • It receives excitatory input from the frontal cortex and has a role in modulating planned motor activity.
194
Q

Which structures are the main input nuclei of the basal ganglia? (LO6+7+8)

A
  • The caudate and putamen.

- Much of the information that the basal ganglia receives comes from the cerebral cortex to these structures.

195
Q

Which structures are the main output nuclei of the basal ganglia? (LO6+7+8)

A
  • The globus pallidus and the substantia nigra.
  • They send projections out from the basal ganglia to the cerebral cortex, mostly via the thalamus, as well as to nuclei in the brainstem.
196
Q

What is the function of the basal ganglia? (LO6+7+8)

A
  • The cerebral cortex comes up with the overall plan of the motor activity and sends the plan down via the basal ganglia, into the spinal cord.
  • When the plan needs to be modulated, this is where the basal ganglia comes in.
  • Activity in the nuclei of the basal ganglia doesn’t cause movement independently but instead, the basal ganglia influence activity in other areas of the brain like the motor cortex to effect movement.
  • The ways in which the basal ganglia do this is not fully understood.
197
Q

Describe the hypothesis regarding how the basal ganglia work. (LO6+7+8)

A
  • There are different circuits in the basal ganglia that inhibit and promote movement respectively.
  • According to this theory, the main output of the basal ganglia is inhibitory and neurones in the globus pallidus are constantly inhibiting the thalamus to prevent unwanted movements.
198
Q

What are the three pathways of movement control in the basal ganglia? (LO6+7+8)

A
  • Hyperdirect pathway - promotes movement.
  • Direct pathway - promotes movement.
  • Indirect pathway - inhibits movement.

It is thought that the balance between activity in the direct and indirect pathways allows for smooth movement.

199
Q

Describe the process of the hyperdirect pathway in movement control in the basal ganglia. (LO6+7+8)

A
  1. Motor cortex sends planned movement information to subthalamic nucleus.
  2. Subthalamic nucleus sends this information to globus pallidus.
  3. Globus pallidus inhibits the thalamus.
  4. The natural state of the thalamus is in inhibition of the motor cortex. So when the thalamus is inhibited, the motor cortex is allowed to initiate the planned movement.
200
Q

Describe the process of the direct pathway in movement control in the basal ganglia. (LO6+7+8)

A
  1. Motor cortex sends planned movement information to striatum (outside basal ganglia).
  2. Striatum inhibits substantia nigra and globus pallidus.
  3. Substantia nigra and globus pallidus inhibit the thalamus.
  4. The natural state of the thalamus is in inhibition of the motor cortex. So when the thalamus is inhibited, the motor cortex is allowed to initiate the planned movement.
201
Q

Describe the process of the indirect pathway in movement control in the basal ganglia. (LO6+7+8)

A
  1. Motor cortex sends information about movement to striatum (outside basal ganglia).
  2. Striatum inhibits globus pallidus external (GPe). The natural state of the GPe is in inhibition of the subthalamic nucleus so the neurones in the subthalamic nucleus have the potential to be activated.
  3. Motor cortex sends information about movement to subthalamic nucleus.
  4. Subthalamic nucleus sends information to globus pallidus internal (GPi) and substantia nigra pars reticulata.
  5. GPi and subtantia nigra pars reticulata inhibit the thalamus.
  6. The inhibition of thalamic neurones inhibits the motor cortex and inhibits movement.
202
Q

Describe the role of the cerebellum in movement. (LO6+7+8)

A
  • Adjusts motor responses by comparing the intended output with sensory signals.
  • Updates movement commands if they deviate from the intended trajectory.
  • Facilitates movement by identifying errors during movement and corrects them, allowing for fluid-type movement.

MBBS - Y1 (14 decks)

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