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UMN vs LMN Lesions

Overview

• Upper Motor Neuron (UMN): Cell bodies in the motor cortex (precentral gyrus); axons travel via the corticospinal and corticobulbar tracts to synapse on lower motor neurons. Also includes brainstem neurons that control spinal motor neurons.
• Lower Motor Neuron (LMN): Cell bodies in the anterior horn of the spinal cord (or cranial nerve motor nuclei for the head); axons travel via peripheral nerves directly to skeletal muscle.

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Comparison Table

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Key Features Explained

UMN Lesions

• Spasticity: Velocity-dependent increase in tone (catches when you move the limb quickly). Caused by damage to descending inhibitory pathways that travel alongside the corticospinal tract, leading to increased excitability of anterior horn motor neurons.
• Hyperreflexia: Exaggerated stretch reflexes (e.g., brisk knee jerk, ankle clonus).
• Babinski sign: Dorsiflexion of the great toe + fanning of other toes on stroking the lateral sole. Normal in infants (corticospinal tract not yet myelinated); pathological in adults.
• No significant atrophy: The LMN and muscle are intact; only mild disuse wasting develops over time.
• Pyramidal distribution: In the arm, flexors are relatively stronger (extensors weak); in the leg, extensors are relatively stronger (flexors weak) - producing the classic hemiplegic posture/gait.
• Important caveat: Acute UMN lesions (e.g., acute stroke, acute spinal cord injury / spinal shock) initially produce flaccid paralysis with decreased tone and decreased reflexes. Spasticity develops over hours to months as the cord adapts.

LMN Lesions

• Flaccid paralysis: Loss of all motor neuron influence on the muscle - no tone, no reflex arc.
• Atrophy: Early and severe; the muscle loses its trophic supply from the motor neuron.
• Fasciculations: Visible/palpable muscle twitches caused by spontaneous discharge of a denervated motor unit. A classic sign of LMN disease (e.g., ALS, radiculopathy).
• Areflexia: The reflex arc (LMN → muscle) is broken.
• Segmental/distal distribution: Weakness matches the territory of the affected nerve root, peripheral nerve, or anterior horn segment.

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Pathophysiology Summary

Cerebral cortex
      ↓
  [UMN] corticospinal tract
      ↓
Anterior horn (spinal cord) or cranial nerve nucleus
      ↓
  [LMN] peripheral nerve
      ↓
    Muscle

• Damage above the anterior horn cell = UMN signs
• Damage at or below the anterior horn cell = LMN signs

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Special Situations

Facial Nerve (CN VII)

• UMN lesion (e.g., stroke): Contralateral lower face weakness only. The upper face is spared because it receives bilateral cortical input (both hemispheres contribute to forehead movement).
• LMN lesion (e.g., Bell's palsy): Entire ipsilateral face is weak - upper and lower.

Combined UMN + LMN (e.g., ALS)

• Amyotrophic Lateral Sclerosis destroys both anterior horn cells (LMN - atrophy, fasciculations) and corticospinal tracts (UMN - spasticity, hyperreflexia). This combination of fasciculations + brisk reflexes in a wasted limb is pathognomonic.

Spinal Cord Lesions

• At the level of injury: LMN signs (anterior horn cell damage)
• Below the level of injury: UMN signs (corticospinal tract interruption)

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Quick Memory Aid

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Myocardial Infarction (MI)

Definition

• Myocyte dysfunction begins within 1-2 minutes of ischemia
• Irreversible cell death occurs after 20-40 minutes
• The infarct achieves its full extent in 3-6 hours - the critical therapeutic window

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Pathogenesis

1. Atherosclerotic plaque disruption or erosion - exposes subendothelial collagen and necrotic plaque contents
2. Platelet adhesion and aggregation - release of TXA₂, ADP, serotonin → further aggregation + vasospasm
3. Coagulation cascade activation via exposed tissue factor → growing thrombus
4. Complete coronary occlusion within minutes

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Patterns of Infarction

By depth

• Transmural - full thickness of ventricle wall; caused by epicardial vessel occlusion + thrombosis
• Subendocardial - inner one-third only; thrombus lysed before necrosis becomes transmural, or demand ischemia (tachycardia, hypotension, anemia) on a background of fixed stenosis

By vessel territory (Robbins)

Subendocardial muscle is most vulnerable because: (1) it is the last area to receive blood from epicardial vessels, and (2) intramural pressure during systole compresses its vessels intensely.

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Morphological Timeline (Robbins - Table 9.2)

Healing progresses from border to center. Large infarcts heal more slowly. Old scars (8 weeks or 10 years old) look identical.

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ECG Changes

• (A) Normal
• (B) Very early (hours): ST elevation in I, aVL, V3-5; reciprocal ST depression in II, III, aVF
• (C) Hours to days: Q waves appear; ST changes persist; T-wave inversion begins
• (D) Days to weeks: Deep Q/QS; ST near-baseline; deep T inversion
• (E) Weeks to months: Q waves remain (permanent); T waves normalize ("chronic" pattern)

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Biomarkers

• Troponin I / Troponin T - gold standard; most sensitive and specific; rise within 3-4 hours, peak at ~24 hrs (cTnI) or ~48 hrs (cTnT), remain elevated 7-10+ days
• CK-MB - rises within 4-6 hours, peaks at ~24 hours, normalizes by 48-72 hours; useful for detecting reinfarction
• Myoglobin - earliest to rise (~1-2 hours) but not cardiac-specific
• Myocyte membrane disruption is the earliest detectable event, allowing intracellular macromolecules to leak into the interstitium and vasculature

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Complications

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Reperfusion and Reperfusion Injury

• Mitochondrial dysfunction - ischemia alters membrane permeability → swelling → rupture → apoptosis
• Calcium overload - increased intracellular Ca²⁺ → myofibril hypercontracture → cell death
• Free radical burst - O₂⁻, H₂O₂, hydroxyl radicals damage membrane proteins and lipids within minutes of reperfusion
• No-reflow phenomenon - leukocyte aggregation occludes microvasculature, preventing perfusion even after vessel opening
• Stunned myocardium - viable but non-contractile myocytes post-reperfusion; may persist for days

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Key Management Principles

• Aspirin + P2Y12 inhibitor (dual antiplatelet) - inhibit further platelet aggregation
• Primary PCI - reperfusion of choice within 90 minutes of first medical contact
• Thrombolytics - if PCI unavailable within 120 min
• Beta-blockers - reduce myocardial oxygen demand, limit infarct size, anti-arrhythmic
• ACE inhibitors - reduce adverse remodeling and mortality
• Statins - plaque stabilization and LDL reduction
• Anticoagulation - heparin during PCI; prevents mural thrombus
• Riluzole - in ALS-associated motor neuron disease involving glutamate excitotoxicity (separate indication)
• Spasticity from ischemic injury can be treated with baclofen or tizanidine

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Abnormal Uterine Bleeding (AUB)

Definition and Normal Parameters

• Cycle length: 24-38 days
• Duration of flow: 4-8 days (>7 days = abnormal)
• Average blood loss: 35 mL per cycle; >80 mL = abnormal (heavy menstrual bleeding)

The term "dysfunctional uterine bleeding (DUB)" is no longer recommended. The current standard term is AUB with PALM-COEIN classification (FIGO 2011, endorsed by ACOG).

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PALM-COEIN Classification (FIGO 2011)

PALM - Structural Causes

COEIN - Non-structural Causes

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Causes by Age Group (Robbins)

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Pathophysiology of Key Causes

Anovulatory Bleeding (most common, ~50% of cases)

• No ovulation → no corpus luteum → no progesterone produced
• Unopposed estrogen → endometrium proliferates excessively → becomes unstable → breaks down irregularly and unpredictably
• Most common at: menarche and perimenopause (HPO axis fluctuation), and in PCOS

Fibroids (Leiomyomata)

• Submucosal fibroids are most problematic: increased endometrial surface area + disruption of uterine contraction mechanism → vessel compression fails → heavy bleeding

Endometrial Hyperplasia

• Estrogen excess (obesity, PCOS, granulosa cell tumors, exogenous estrogens) → endometrial gland proliferation
• Without atypia: 1-3% risk of progression to carcinoma
• With atypia (EIN): associated with PTEN mutations; considered a carcinoma precursor; requires hysterectomy (or high-dose progestins if fertility preservation needed)

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Workup / Investigation

• Detailed menstrual history and pelvic exam
• Pregnancy test (urine/serum β-hCG) - exclude first
• CBC (anemia assessment)
• Thyroid function tests (hypothyroidism causes menorrhagia)
• Prolactin level (hyperprolactinemia disrupts GnRH → LH/FSH reduction → anovulation)
• Cervical cancer screening (if not current)
• STI screening
• Pelvic ultrasound - first-line imaging

• Heavy bleeding since menarche
• Family history of coagulopathy
• Medication-associated bleeding
• Signs of systemic bleeding (epistaxis, easy bruising)

• Age ≥45 years with AUB (including intermenstrual bleeding)
• Age <45 with risk factors: obesity, unopposed estrogen, ovulatory dysfunction, persistent/refractory AUB, elevated familial cancer risk (Lynch syndrome, Cowden syndrome)

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Management

Medical (First-line for non-structural causes)

Surgical

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Special Scenarios

Postmenopausal Bleeding

• Always abnormal - requires thorough evaluation
• Most common cause: endometrial atrophy (not carcinoma)
• Most feared cause: endometrial carcinoma (endometrioid type in 80% - estrogen-related; serous type in 15% - atrophy-related, more aggressive)
• Workup: pelvic ultrasound (endometrial thickness), EMB

Acute Heavy Bleeding (Emergency Department)

• IV conjugated estrogen for rapid hemostasis
• High-dose OCP regimens
• Tranexamic acid
• If hemodynamically unstable: resuscitation, urgent gynaecology consult, possible surgical intervention

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