Module 5 readings: abnormal gait, endocrine and metabolic disorders, CRPS, neuro disorders, prosthesis and gait)

Contracture vs. Weakness Effect on ROM

Contracture leads to decreased ROM of the opposite motion; weakness leads to decreased ROM of the same motion.

Short Leg Characteristics (LLD)

Associated with plantar flexion and inversion.

Long Leg Characteristics (LLD)

Associated with dorsiflexion, eversion, and knee flexion.

Backward Trunk Lean in Stance Phase is caused by

Caused by weak hip extensors (gluteus maximus) or rigid hip flexion contracture to maintain hip extension and reduce muscle demand.

Backward Trunk Lean in Swing Phase is caused by

Caused by hip flexor weakness to passively assist in forward advancement of the limb.

Forward Trunk Lean in Stance Phase is caused by

Caused by hip flexion contracture, weak quadriceps, or plantar flexor contracture/spasticity to reduce joint demands and shift the center of mass.

Ipsilateral Trunk Lean (Compensated Trendelenburg) is caused by

Lateral trunk lean toward the stance leg caused by marked hip abductor weakness, hip arthritis pain, ITB tightness, or scoliosis.

Contralateral Trunk Lean

Lateral trunk lean to the opposite leg during swing phase, compensating to lift the pelvis for foot clearance (typically seen with LLD).

Positive Trendelenburg Sign / Contralateral Pelvic Drop

Pelvic drop of the swing leg during stance phase caused by ipsilateral hip abductor weakness, hip adductor spasticity, or contracture.

Ipsilateral Pelvic Drop

Pelvic drop during swing phase caused by contralateral hip abductor weakness, hip adductor spasticity, or contracture.

Excessive Plantar Flexion in Gait

Occurs in MSt/TSt; caused by PF contracture, spasticity, or fused ankle. Results in forefoot IC and early heel-off.

Excessive Dorsiflexion in Gait caused by

Occurs in MSt/TSt; caused by inability of PFs to control tibial advancement, knee/hip flexion contractures, or fixed DF deformity. Results in late heel-off.

Foot Slap is caused by

Rapid ankle plantar flexion after heel strike in LR caused by mild dorsiflexor weakness.

Foot Flat is and caused by

Entire plantar aspect of foot contacts ground at IC; caused by marked dorsiflexor weakness, PF contracture, or knee flexion contracture.

Excessive Inversion in Gait

Subtalar inversion during stance/swing caused by overactive/contracted invertors, evertor weakness, or primitive extensor pattern.

Excessive Eversion in Gait

Subtalar eversion during stance/swing caused by overactive/contracted evertors, invertor weakness, or primitive flexor pattern.

Toes or Forefoot Contact at IC

Caused by LLD, PF contracture/spasticity, severe DF weakness, painful heel, or excessive knee flexion.

Toe Clawing in Stance Phase is caused by

Caused by toe flexor spasticity, excessive toe flexor activation for PF weakness, or primitive reflexes.

Excessive Knee Flexion in Stance Phase is caused by

Caused by knee flexion deformity, hamstring spasticity, pain/effusion, proprioceptive loss, or PF weakness.

Excessive Knee Flexion in Swing Phase caused by

Compensatory strategy for toe clearance caused by stance limb shortness or lack of swing limb ankle DF.

Knee Extension in Stance Phase caused by

Caused by weak quadriceps or knee pain; often accompanied by anterior trunk lean to keep the knee extended without quad action.

Knee Thrust is and caused by

Rapid knee extension occurring after IC, caused by quadriceps spasticity.

Knee Hyperextension occurs when due to what

Occurs in stance/swing due to weak quadriceps (stretching posterior structures) or PF contracture/spasticity (compensating for lack of tibial advancement).

Excessive Hip Flexion in Stance & Swing caused by

Stance cause: weak extensors or severe contractures. Swing cause: long limb, flexor synergy, or lack of DF for toe clearance.

Limited Hip Flexion occurs when and caused by what

Occurs in stance/swing; caused by weak hip extensors/flexors or hamstring contracture/spasticity.

Hip Circumduction caused by what

Lateral circular movement of the swing leg (abduction/ER followed by adduction/IR) caused by hip flexor weakness or inability to shorten the leg.

Hip Hiking caused by

Compensatory swing phase strategy to lift the foot using pelvis elevation, caused by limited hip/knee flexion or lack of DF.

Scissoring Gait (Excessive Adduction)

Adducted femur position during all phases; caused by hip adductor contracture/spasticity or contralateral pelvic drop.

Right Hip Abductor Weakness Trendelenburg Effect

Results in left pelvic drop (contralateral drop).

Left Hip Abductor Weakness Trendelenburg Effect

Results in right pelvic drop (contralateral drop).

what does the hypothalamus do?

Hypothalamus

● Regulates the autonomic nervous system (ANS) and helps maintain body homeostasis

➤ Manages temperature, sweat, sexual behavior, thirst, fear, blood pressure (BP),

sleep

➤ Controls the release of pituitary hormones through

Corticotropin-releasing hormone (CRH)

Thyrotropin-releasing hormone (TRH)

Growth-hormone-releasing hormone (GHRH)

Somatostatin

● Mnemonic: The hypothalamus tells a "TALE" = Temperature, Appetite, Libido,

Emotion

What hormones are released by the anterior pituitary gland?

Growth hormone (GH), adrenocorticotropic hormone (ACTH), follicle-stimulating hormone (FSH), prolactin, luteinizing hormone (LH), and thyroid-stimulating hormone (TSH).

What hormones are released by the posterior pituitary gland?

Antidiuretic hormone (ADH) and oxytocin.

What is the function of thyroid-stimulating hormone (TSH) from the pituitary gland?

It stimulates the thyroid gland to release thyroxine (T4) and triiodothyronine (T3).

What do the follicular cells of the thyroid gland secrete and regulate?

They secrete thyroxine (T4) and triiodothyronine (T3), which help regulate metabolism and protein synthesis.

What is the function of C cells in the thyroid gland?

They secrete calcitonin, which affects calcium and phosphorus homeostasis.

What do the parathyroid glands release and what is its role?

They release parathyroid hormone (PTH), which regulates calcium and phosphate homeostasis in the blood and the calcification of bone.

What is the role of aldosterone released via the adrenal cortex?

It regulates potassium and sodium levels and maintains fluid and electrolyte balances.

What are the functions of cortisol released by the adrenal cortex?

It regulates carbohydrate metabolism, aids immune function, reduces inflammation, and promotes gluconeogenesis.

What do androgens and androstenedione from the adrenal cortex regulate?

Sexual functions.

What hormones does the adrenal medulla release and what are their effects?

Epinephrine and norepinephrine; they support the fight-or-flight response, increase blood glucose levels, and stimulate ACTH production.

What hormones are secreted by the Islets of Langerhans in the pancreas?

Insulin, glucagon, and amylin.

What is the function of insulin?

It lowers blood glucose levels and increases the use of carbohydrates.

What is the function of glucagon?

It stimulates glucose production by the liver to increase glucose levels, especially in the fasting state.

What is the function of amylin?

It delays gastric emptying and suppresses the release of glucagon.

What role do the kidneys play in hormone-related processes?

They convert vitamin D to its active form.

What hormones do the ovaries secrete?

Estrogen and progesterone.

What is the function of estrogen?

It regulates female reproductive organs, controls female sexual characteristics, and is involved in the menstrual cycle and pregnancy.

What is the function of progesterone?

It stimulates breast tissue for lactation and prepares the endometrium for implantation of the fertilized ovum.

What do the testes secrete and control?

They secrete androgens (testosterone), which control male sexual characteristics.

What is metabolic syndrome (syndrome X)?

A collection of risk factors that increase the risk of heart disease, stroke, and diabetes mellitus (DM).

How many risk factors are required to diagnose metabolic syndrome?

Diagnosis requires 3 or more of the specified risk factors.

Metabolic Syndrome: Abdominal Obesity Criteria

Waist circumference ≥ 40 in (> 102 cm) for males or ≥ 35 in (> 89 cm) for females.

Metabolic Syndrome: High Triglyceride Criteria

Triglyceride levels ≥ 150 mg/dL.

Metabolic Syndrome: HDL Cholesterol Criteria

< 40 mg/dL in males or < 50 mg/dL in females.

Metabolic Syndrome: High Blood Pressure Criteria

Systolic blood pressure (SBP) ≥ 130 mmHg, diastolic blood pressure (DBP) ≥ 85 mmHg.

Metabolic Syndrome: Blood Sugar Criteria

Fasting plasma glucose ≥ 100 mg/dL.

What are the dominant underlying risk factors for metabolic syndrome?

Sedentary lifestyle with little to no physical activity, abdominal obesity, and insulin resistance.

What lifestyle modifications help manage metabolic syndrome?

Healthy diet, weight loss, exercise, and smoking cessation.

What medications are considered in metabolic syndrome management?

Medications to control cholesterol, blood pressure, and diabetes mellitus (DM).

What is Diabetes Mellitus (DM)?

A chronic disorder of carbohydrate, fat, and protein metabolism due to insufficient or defective insulin action.

What is the primary cause of Diabetes Mellitus?

Abnormally high levels of sugar or glucose in the blood.

Which populations have a higher prevalence of Diabetes Mellitus?

Native American, Hispanic or Latino, Native Hawaiian, and Pacific Islander individuals.

What are the key characteristics of Type 1 DM?

Insulin-dependent, juvenile-onset (5%-10% of cases) with little or no insulin produced due to decreased islet cell size.

What is the typical age and onset pattern of Type 1 DM?

Abrupt onset, peaking at puberty and usually occurring at under 30 years of age.

What is the etiology and risk factors for Type 1 DM?

Autoimmune, environmental, and genetic factors, with possible viral factors causing islet cell destruction.

How do ketone bodies affect arterial pH in ketoacidosis?

They alter arterial pH to become more acidic (decrease pH).

What is Kussmaul breathing a sign of?

Diabetic ketoacidosis (DKA).

What is hyperparathyroidism and what does it disrupt?

Excessive secretion of PTH; disrupts calcium, phosphate, and bone metabolism.

What are the effects of hyperparathyroidism on serum calcium and phosphate?

Increases serum calcium and decreases serum phosphate.

How does hyperparathyroidism affect bones and kidneys?

Takes calcium from bones (demineralizing them); increased serum calcium can cause kidney stones.

What are the clinical manifestations of hyperparathyroidism?

Fatigue, drowsiness, confusion, poor memory, slowed mentation, myalgias, depression, sensory loss, hyperactive DTRs, osteopenia, gout/pseudogout, proximal muscle weakness, arthralgia, nausea, vomiting, constipation, peptic ulcers, pancreatitis, and kidney stones.

What does the mnemonic "Moans, groans, stones, and bones" stand for in hyperparathyroidism?

"Moans" = mental problems; "Groans" = myalgia, arthralgia, gout; "Stones" = kidney stones; "Bones" = bone decalcification.

What is the treatment for hyperparathyroidism?

Surgical removal of the gland.

What characterizes Addison's disease and what are its etiologies?

Decreased production of cortisol and aldosterone; etiologies include autoimmune processes, infection, neoplasm, hemorrhage, and medications like antifungals, etomidate, and phenytoin.

What are the key signs and symptoms of Addison's disease?

Dark skin pigmentation, postural hypotension, progressive fatigue, hyperkalemia, GI disturbances, nausea, vomiting, arthralgias, myalgias, tendon calcification, and hypoglycemia.

What is the acute treatment for adrenal insufficiency in Addison's disease?

Replacement therapy including fluids, electrolytes, glucose, and cortisol, along with identification of the underlying cause.

What is the treatment for chronic adrenal insufficiency?

Lifelong administration of corticosteroids and mineralocorticoids.

What causes secondary adrenal insufficiency?

A lack of pituitary ACTH due to insufficient stimulation of the adrenal cortex, caused by pituitary removal, rapid drug withdrawal, or tumors.

What is Cushing syndrome?

Hyperfunction of the adrenal gland characterized by increased secretion of cortisol by the adrenal cortex.

What are the primary functions of cortisol?

It increases the release of stored glucose, stops digestion during fight-or-flight, and suppresses the immune system.

What are the common signs and symptoms of Cushing syndrome?

Moon face, buffalo hump, truncal obesity, muscle wasting, decreased bone density, HTN, kyphosis, easy bruising, psychiatric disturbances, impaired reproductive function, DM, slow wound healing, masculinizing effects in females, thinning hair, and hypokalemia.

What are the treatment approaches for Cushing syndrome?

Decreasing excess ACTH via irradiation or surgery, a high-protein diet for muscle wasting, electrolyte and fluid balance, and lifelong glucocorticoids following adrenal resection.

difference between fibromyalgia vs myofascial pain syndrome

fibromyalgia: pain in muscles, postural stress, dec ROM, tender pts at specific sites, no referred pattern pain, no tight band in muscle, fatigue and walking unrefreshed, morning stiffness

myofascial pain: pain in muscles, postural stress, dec ROM, trigger pts in muscles, referred pattern pains, tight band in muscles, no related fatigue complaints

What event typically precedes the development of CRPS Type 1 (Reflex Sympathetic Dystrophy)?

An initiating noxious event such as a crush, soft tissue injury, immobilization, tight cast, or surgery.

What is a key distinguishing characteristic of CRPS Type 2 (Causalgia)?

It develops after a nerve injury.

How do symptoms of CRPS typically distribute and progress in an extremity?

Symptoms are more marked distally and progress in intensity while spreading proximally.

What is the relationship between CRPS symptoms and the inciting event?

There is a disproportion of symptoms in relation to the causing event.

What is considered the key feature and primary symptom of CRPS?

Pain, along with sensory abnormalities such as burning pain and allodynia.

What sudomotor and edema impairments are commonly seen in CRPS?

Edema and/or sweating changes or asymmetry, including hyper or hypohydrosis.

What characterizes vasomotor instability impairments in CRPS?

Temperature asymmetry and/or skin color changes and asymmetry.

What are the common trophic changes associated with structural impairments in CRPS?

Increased or decreased hair and nail growth and skin changes like thin or shiny skin.

How do pain avoidance behaviors impact the involved limb in chronic stages of CRPS?

They cause decreased limb use, leading to muscle atrophy or osteoporosis/osteopenia.

What motor execution characteristics are common in individuals with CRPS?

Slower movement initiation and slower, more inaccurate execution of targeted movements.

Parkinson Disease Pathophysiology

Depletion of dopamine from the substantia nigra in the basal ganglia, leading to excessive cholinergic excitation.

TRAP Mnemonic for Parkinson Disease

Resting Tremor, Rigidity, Akinesia/Bradykinesia, and Postural instability.

Cogwheel vs. Lead-Pipe Rigidity

Cogwheel is jerky ratchetlike resistance with tremor; lead-pipe is sustained resistance with no fluctuations.

Festinating Gait Characteristics

Progressive increase in speed with short strides, stooped posture, and inability to stop on command.

Rolling Walker Contraindication in PD

Contraindicated due to forward festinating gait and tendency to accelerate forward.

Festinating Gait Treatment

Use a toe wedge or flat heel to displace the center of gravity posteriorly.