Stroke: Types, Mechanisms, and Lacunar Infarct

What Is a Stroke?

• Park's Textbook of Preventive and Social Medicine
• Bradley and Daroff's Neurology in Clinical Practice

Classification of Stroke

A. Ischemic Stroke (~80% of all strokes)

1. In Situ Occlusive Stroke

• Large artery (Atherothrombotic infarction): Atherosclerosis affects major vessels (carotid bifurcation, MCA stem, vertebrobasilar system). Mechanism is usually artery-to-artery embolization or thrombosis, often triggered by plaque rupture/ulceration. Risk factors: hypertension, diabetes, smoking, hyperlipidemia. - Bradley and Daroff's Neurology
• Small artery / Penetrating artery disease - LACUNAR INFARCT: (see below in detail)

2. Embolic Stroke

• Emboli travel from a remote source (cardiac or proximal vascular) and lodge in a cerebral artery.
• Onset is sudden with maximal deficit at onset - characteristic feature.
• Can involve multiple vascular territories simultaneously (vs. thrombotic = single territory).
• Most common cardiac cause: Atrial fibrillation (AF) - accounts for 50-65% of cardiogenic emboli.
• Other sources: acute MI, infective endocarditis, mechanical prosthetic valves, rheumatic mitral stenosis, dilated cardiomyopathy, PFO.
• Cardioembolic strokes account for ~15-20% of all ischemic strokes. - Bradley and Daroff's Neurology

3. Watershed (Border Zone) Infarction

• Occurs when systemic hypoperfusion affects the most vulnerable brain regions: the junctional zones between major arterial territories (ACA/MCA/PCA borders).
• Classic presentation: "man in a barrel" syndrome - bilateral arm weakness with leg and face sparing, from ACA-MCA border zone ischemia.
• Also occurs between vertebrobasilar branches (PICA, AICA, SCA territories).
• Cause: global hypoperfusion (e.g., cardiac arrest, severe hypotension, carotid stenosis). - Bradley and Daroff's Neurology

Lacunar Infarct - In Depth

Pathophysiology

Common Sites

• Putamen
• Basis pontis
• Thalamus
• Posterior limb of internal capsule
• Caudate nucleus

Classic Lacunar Syndromes

1. Pure Motor Hemiplegia (PMH) - most common. Lesion in posterior limb of internal capsule or basis pontis. Complete unilateral motor deficit (face, arm, leg) without sensory, visual, or cortical signs.
2. Pure Sensory Stroke (PSS) - lacunar infarct in the ventroposterolateral nucleus of the thalamus. Numbness and paresthesias in a hemisensory distribution (cheiro-oral or cheiro-pedal pattern). Both spinothalamic AND medial lemniscal modalities affected (unlike pontine lesions where they dissociate). - Localization in Clinical Neurology, 8e
3. Sensorimotor Stroke - combined sensory and motor deficits. Lesion typically in posterolateral thalamus + adjacent internal capsule.
4. Ataxic Hemiparesis (AH) - second most common. Lesion in posterior limb of internal capsule, basis pontis, or corona radiata. Features: ipsilateral leg/foot weakness + homolateral cerebellar ataxia disproportionate to the motor deficit. No cortical signs, visual field defects, or dysarthria. - Localization in Clinical Neurology, 8e
5. Dysarthria-Clumsy Hand Syndrome - dysarthria + facial weakness + clumsiness of one hand. Basis pontis or genu of internal capsule.

Imaging

• Acute: Hyperintense on DWI (restricted diffusion), hypointense on ADC map.
• Chronic/cavitated: Hypointense on T1, hyperintense on T2/FLAIR with a FLAIR-dark core and hyperintense rim.

Risk Factors and Management

• Long-standing arterial hypertension and diabetes mellitus are the strongest risk factors.
• Also: smoking, dyslipidemia.
• Management: antihypertensive therapy (critical), intensive statin therapy, antiplatelet agents.
• Prognosis: Short-term recovery is more favorable compared to other ischemic stroke subtypes. Some patients achieve complete recovery even after severe events, though long-term sequelae can occur. - Frameworks for Internal Medicine

Important: A lacunar syndrome in a hypertensive/diabetic patient is NOT sufficient alone to diagnose lacunar infarct. Other causes (cardioembolic, large artery disease) must be excluded - especially if sensorimotor stroke, sudden onset with AF, or large striatocapsular infarctions are present. - Bradley and Daroff's Neurology

B. Hemorrhagic Stroke (~20% of all strokes)

1. Spontaneous Intracerebral Hemorrhage (ICH)

• Ganglionic (deep): Most commonly due to hypertension causing hyaline arteriolosclerosis and rupture of small penetrating arteries. Typical sites: putamen, thalamus, pons, cerebellum.
• Lobar: Most commonly due to cerebral amyloid angiopathy (CAA), especially in elderly. - Robbins, Cotran & Kumar

2. Subarachnoid Hemorrhage (SAH)

• Blood in the subarachnoid space. Classically described as "thunderclap headache" (worst headache of life).
• Most commonly caused by rupture of a saccular (berry) aneurysm or arteriovenous malformation (AVM).

3. Intracranial Aneurysm

• Saccular aneurysms at arterial bifurcations of the Circle of Willis.
• Rupture causes SAH. Risk increases with hypertension, smoking, polycystic kidney disease.

4. Arteriovenous Malformation (AVM)

• Congenital tangle of arteries and veins without intervening capillaries.
• Risk of rupture causing SAH or intracerebral hemorrhage.

Summary Table

Clinical Symptoms of All Stroke Types - Detailed

General Warning Symptoms (Any Stroke)

• Face drooping (asymmetric smile or facial droop)
• Arm weakness (one arm drifts down when raised)
• Speech difficulty (slurred, garbled, unable to speak or understand)
• Time to call emergency services

I. ISCHEMIC STROKE - Clinical Symptoms by Territory

A. Middle Cerebral Artery (MCA) Stroke - Most Common

• Contralateral hemiplegia (face + arm + leg, but face and arm worse than leg)
• Contralateral hemianesthesia (hemisensory loss)
• Homonymous hemianopia (loss of same visual field both eyes)
• Conjugate ipsilateral eye deviation (eyes deviate toward the stroke side - "looking at the lesion")
• Global aphasia (dominant hemisphere - total loss of speech production and comprehension)
• Hemineglect (nondominant hemisphere - ignores contralateral side of space)

• Hemiparesis predominantly affecting face and arm more than leg
• Broca's aphasia (dominant hemisphere) - nonfluent, broken speech, preserved comprehension
• Impaired prosody (nondominant)

• Wernicke's aphasia (dominant) - fluent but meaningless speech, poor comprehension
• Behavioral disturbances (nondominant)
• Homonymous hemianopia or inferior quadrantanopia

• Pure motor hemiparesis (internal capsule involvement) - no cortical signs

• Alexia with agraphia (left angular gyrus)
• Gerstmann syndrome (dominant parietal): finger agnosia, acalculia, right-left disorientation, agraphia

• Anosognosia (denies having hemiparesis)
• Tactile and visual extinction, hemi-inattention
• Apraxia, impaired prosody, acute agitated delirium
• Bradley and Daroff's Neurology in Clinical Practice

B. Anterior Cerebral Artery (ACA) Stroke - <3% of infarcts

• Contralateral weakness primarily in the lower extremity (leg >> arm) - opposite pattern to MCA
• Abulia (lack of motivation, slowness of thought and action)
• Akinetic mutism (bilateral mesiofrontal damage) - patient is awake but profoundly unresponsive
• Impaired memory or emotional disturbances
• Transcortical motor aphasia (dominant hemisphere) - like Broca's but repetition is preserved
• Deviation of head and eyes toward the lesion
• Paratonia (gegenhalten) - involuntary resistance to passive limb movement
• Discriminative and proprioceptive sensory loss (primarily lower extremity)
• Sphincter incontinence
• Left arm apraxia (anterior corpus callosum disconnection)
• Basal branch infarction: memory disorders, anxiety, agitation
• Bradley and Daroff's Neurology in Clinical Practice

C. Posterior Cerebral Artery (PCA) Stroke

• Homonymous hemianopia (contralateral) - often the dominant symptom; macular vision may be spared
• With dominant hemisphere: alexia without agraphia (can write but cannot read), anomia, memory disturbances
• With nondominant hemisphere: neglect, visuospatial deficits
• Prosopagnosia (bilateral): inability to recognize familiar faces
• Anton syndrome (cortical blindness with denial of blindness)

• Somnolence, peduncular hallucinosis (vivid visual hallucinations), memory disturbance, agitated delirium
• Unilateral or bilateral paralysis of vertical gaze
• Bilateral homonymous hemianopia / cortical blindness
• Thalamic involvement: sensory deficits
• Bradley and Daroff's Neurology in Clinical Practice

D. Vertebrobasilar Stroke

• Ipsilateral: facial pain/numbness (CN V), Horner syndrome (ptosis, miosis, anhidrosis), ataxia, hoarseness/dysphagia (CN IX/X), loss of taste
• Contralateral: loss of pain and temperature in the body/limbs (spinothalamic)
• Vertigo, nausea, vomiting, nystagmus (vestibular nuclei)
• Motor strength is preserved (corticospinal tracts spared)

• Vertigo, nausea, vomiting, nystagmus
• Ipsilateral: facial hyalgesia, corneal hyesthesia, deafness, facial paralysis, Horner syndrome, ataxia
• Contralateral: trunk/extremity loss of pain and temperature

• Vertigo (less common than AICA)
• Ipsilateral: Horner syndrome, ataxia, intention tremor, choreiform dyskinesias
• Contralateral: hearing loss, trunk/extremity hypalgesia and thermoanesthesia (spinothalamic)
• Nystagmus (MLF involvement)

• Coma, quadriplegia
• Locked-in syndrome (if basis pontis bilaterally affected): complete paralysis except vertical eye movements, consciousness preserved
• Cranial nerve palsies, bilateral Babinski signs
• Respiratory failure, death if not treated emergently
• Bradley and Daroff's Neurology in Clinical Practice

E. Lacunar Infarct - Symptoms by Syndrome

• Bradley and Daroff's Neurology in Clinical Practice; Localization in Clinical Neurology 8e

F. Watershed (Border Zone) Infarction

• ACA-MCA border zone: "Man in a barrel" - proximal arm weakness with preserved hand and leg; bilateral arm weakness if bilateral
• MCA-PCA border zone: Visuospatial deficits, dyslexia, dyscalculia, dysgraphia, verbal and nonverbal memory deficits
• Bilateral parieto-occipital: Cortical blindness (improving), inferior altitudinal field defects, optic ataxia, difficulty judging size/distance/movement (Balint syndrome elements)

II. HEMORRHAGIC STROKE - Clinical Symptoms

A. Hypertensive Intracerebral Hemorrhage (ICH) - by Location

• Symptoms are progressive over minutes to hours (versus sudden maximal deficit at onset in embolic stroke)
• Neurologic deficit is never transitory - no TIA-like fluctuation
• More commonly accompanied by headache and vomiting
• Clinical features rarely reliably distinguish ICH from ischemic stroke - imaging is required

• Contralateral hemiplegia (from internal capsule transection) - consistent in medium/large clots
• Vomiting in ~50%
• Headache (frequent but not invariable)
• Face sags on one side, slurred or aphasic speech
• Ipsilateral eye deviation (conjugate deviation away from the paretic limbs)
• Large bleeds: progressive stupor → coma, bilateral Babinski signs, decerebrate rigidity, dilated fixed pupils, irregular respiration

• Severe contralateral sensory loss (entire body including trunk) - cardinal feature
• Hemiplegia/hemiparesis (from adjacent internal capsule compression)
• Fluent aphasia or anomia (dominant side)
• Contralateral neglect (nondominant)
• Homonymous hemianopia (usually transient)
• Ocular signs (highly characteristic of thalamic hemorrhage):
  • Eyes deviate downward and inward ("setting-sun" gaze)
  • Vertical gaze palsy
  • Skew deviation (ipsilateral eye higher)
  • Absent light reaction, retraction nystagmus
  • Ipsilateral Horner syndrome
• Hydrocephalus from third ventricle compression

• Deep coma within minutes - almost invariable
• Total paralysis, bilateral Babinski signs
• Decerebrate rigidity
• Pinpoint pupils (1 mm) that react to light - pathognomonic
• Impaired or absent lateral eye movements (head turning/calorics)
• Death usually within hours; small tegmental bleeds may survive

• Develops over minutes to hours; loss of consciousness at onset is unusual (distinguishing feature from pontine)
• Repeated vomiting - prominent feature
• Occipital headache
• Severe vertigo
• Inability to stand, sit, or walk - patient falls to the affected side
• Note: early examination may appear near-normal; always test gait
• Ipsilateral facial weakness, paresis of conjugate lateral gaze, CN VI weakness (with larger bleeds)
• Dysarthria, dysphagia (variable)
• Risk: sudden brainstem compression with apnea - surgically reversible if caught early

• Occipital: pain around ipsilateral eye + dense homonymous hemianopia
• Temporal: pain in/anterior to ear + partial hemianopia + fluent aphasia
• Frontal: frontal headache + contralateral hemiplegia (arm predominantly)
• Parietal: anterior temporal headache + contralateral hemisensory deficit
• Progressive worsening headache + vomiting + drowsiness accompanying any focal syndrome = virtually diagnostic of hemorrhage
• Adams and Victor's Principles of Neurology, 12th Edition

B. Subarachnoid Hemorrhage (SAH)

• "Thunderclap" headache - sudden, cataclysmic, peaks within seconds to minutes; described as "worst headache of my life." Headaches that take >60 minutes to peak are unlikely to be SAH.

• Syncope (may be the initial manifestation, with headache beginning as consciousness returns)
• Nausea and vomiting
• Meningism: neck stiffness, photophobia, phonophobia
• Seizures
• Up to 20% have focal neurologic deficits
• Oculomotor (CN III) palsy: complete ptosis + "down-and-out" eye + dilated pupil = posterior communicating artery aneurysm compressing CN III
• CN VI palsy
• ~50% have altered or fluctuating consciousness

• Up to 1/3 of patients recall a preceding milder headache ("warning leak") days to weeks before the major SAH

• Rosen's Emergency Medicine; Localization in Clinical Neurology 8e

Quick Differentiation Summary

Cortical Signs vs. Non-Cortical (Subcortical) Signs

The Core Concept

1. Cerebral cortex - the outer gray matter where complex, "higher" brain functions are processed (language, perception, praxis, gnosis, spatial awareness)
2. Subcortical structures - white matter tracts, internal capsule, basal ganglia, thalamus, brainstem, cerebellum - which relay or process signals below the cortex

• Cortical lesion = damage to the brain's "processing center" → deficits in language, recognition, skilled movement, spatial awareness
• Subcortical lesion = damage to the brain's "wiring" → motor/sensory pathways interrupted, but the cortex itself is intact, so no higher-function deficits

• Bradley and Daroff's Neurology in Clinical Practice

CORTICAL SIGNS

1. Language Disturbances (APHASIA) - Dominant Hemisphere (Usually Left)

• Harrison's Principles of Internal Medicine 22E; Bradley and Daroff's Neurology

2. Neglect / Hemineglect - Nondominant Hemisphere (Usually Right Parietal)

• Hemispatial neglect - ignores objects/people on the left side of space
• Tactile extinction - can feel each hand individually, but when touched simultaneously, only perceives the right side
• Visual extinction - similar phenomenon in vision
• Anosognosia - unawareness or denial of one's own neurological deficit (e.g., patient insists their paralyzed arm is fine)
• Anosodiaphoria - patient acknowledges deficit but shows no concern about it
• Hemisomatognosia - feels the left limb does not belong to them

3. Visuospatial Deficits - Nondominant (Right) Parietal

• Constructional apraxia - unable to copy drawings or assemble objects (test: draw a clock face or copy a cube)
• Dressing apraxia - cannot dress oneself due to spatial disorientation, not limb weakness
• Loss of topographic memory - cannot recall routes or familiar layouts
• Distortion of visual coordinates - misjudging distances, upside-down reading, visual illusions

4. APRAXIA - Dominant (Left) Parietal or Frontal

• Ideomotor apraxia: Can do the action automatically but cannot do it on command (e.g., "show me how to brush your teeth")
• Ideational apraxia: Fails at sequencing multi-step tasks (cannot make a cup of tea step-by-step)
• Limb-kinetic apraxia: Fine, delicate hand movements are clumsy despite intact strength (frontal)
• Callosal apraxia: Left hand apraxia only - from anterior corpus callosum damage (ACA territory)
• Apraxia of gait (frontal): Difficulty walking despite normal leg strength ("magnetic gait")

5. AGNOSIA - Cortical Recognition Failure

• Visual agnosia - sees an object but cannot identify it (usually bilateral posterior lesions)
• Prosopagnosia - cannot recognize familiar faces (bilateral occipitotemporal)
• Finger agnosia - cannot identify own fingers (part of Gerstmann syndrome)
• Astereognosis - cannot identify an object by touch (parietal cortex)
• Asymbolia for pain - can feel pain but has no emotional/behavioral response to it

6. GERSTMANN SYNDROME - Dominant Left Parietal (Angular Gyrus)

1. Finger agnosia - cannot name or identify fingers
2. Acalculia - inability to calculate
3. Agraphia - inability to write
4. Right-left disorientation - cannot distinguish right from left

7. ALEXIA / AGRAPHIA

• Alexia with agraphia - cannot read or write (left angular gyrus)
• Alexia without agraphia - can write but cannot read (left occipital + splenium of corpus callosum) - "pure alexia"

8. Homonymous Hemianopia

• Cortical hemianopia (occipital lobe): "Macular sparing" hemianopia because macular cortex has dual blood supply
• Subcortical (optic radiation): May produce quadrantanopias

9. Frontal Lobe Cortical Signs

• Abulia - profound loss of motivation, slowness of thought, reduced spontaneous movement
• Akinetic mutism - awake but completely unresponsive, no movement or speech (bilateral mesiofrontal)
• Personality changes / disinhibition - impulsivity, inappropriate behavior (orbitofrontal)
• Paratonia (gegenhalten) - involuntary, variable resistance to passive limb movement
• Primitive reflexes: grasp reflex, sucking reflex, palmomental reflex (release of frontal inhibition)
• Impaired planning, set-shifting, and sequential processing (executive function)
• Bradley and Daroff's Neurology in Clinical Practice

NON-CORTICAL (SUBCORTICAL) SIGNS

What is ABSENT in a subcortical lesion:

• No aphasia
• No apraxia
• No agnosia
• No neglect
• No hemianopia (or only minor visual field changes)
• No anosognosia
• No Gerstmann syndrome

What IS Present:

Why This Distinction Matters in Stroke

Memory Aid

CORTICAL = "Higher Brain" damage
  ↓
FAST + HIGHER:
  F - Fluency/Aphasia
  H - Hemianopia (cortical)
  A - Apraxia
  S - Spatial neglect
  T - Topographic/recognition (agnosia)
  H - Higher personality changes
  E - Expression (Broca) or comprehension (Wernicke)
  R - Right-left confusion (Gerstmann)

SUBCORTICAL = "Pure" signs only
  Motor OR Sensory (or both) — NOTHING ELSE

Diabetes Mellitus - Symptoms and Complications

What Is Diabetes Mellitus?

• Type 1 DM (T1D): Autoimmune destruction of pancreatic beta cells → absolute insulin deficiency
• Type 2 DM (T2D): Insulin resistance + progressive beta-cell failure → relative insulin deficiency
• Other types: Gestational diabetes, MODY, drug-induced, pancreatogenic
• Fuster and Hurst's The Heart, 15th Edition

Clinical Symptoms of Diabetes

Classic Triad (the "3 Polys")

Additional Symptoms

• Weight loss - especially in T1D: catabolism of fat and muscle due to insulin deficiency, glycosuria (calorie loss in urine)
• Fatigue and weakness - cells starved of glucose despite hyperglycemia
• Blurred vision - osmotic changes in the lens (sorbitol accumulation alters lens shape and refractive index)
• Frequent superficial infections (skin, urinary tract, candidal) - impaired phagocyte function (chemotaxis, killing, respiratory burst), glycosuria promotes bacterial growth
• Slow healing of skin wounds - impaired leukocyte function + microvascular disease reduces perfusion
• Nocturia - related to polyuria disrupting sleep

Acute Complications (Presenting Emergencies)

Long-Term (Chronic) Complications

1. Advanced Glycation End Products (AGEs) - glucose metabolites attach to proteins → AGE-RAGE signaling → VEGF, TGF-β release, oxidative stress, procoagulant state, basement membrane thickening
2. Protein Kinase C (PKC) activation - DAG synthesis from glycolytic intermediates → VEGF, TGF-β, PAI-1 production → microangiopathy
3. Polyol pathway flux (Aldose reductase) - glucose → sorbitol → depletes NADPH → impairs glutathione regeneration → oxidative stress; sorbitol accumulates in lens (cataracts), nerves
4. Hexosamine pathway flux - excess fructose-6-phosphate → oxidative stress → insulin resistance, vascular complications

MICROVASCULAR COMPLICATIONS

1. Diabetic Retinopathy

• Microaneurysms - earliest sign; small outpouchings of retinal capillaries (appear as tiny red dots on fundoscopy)
• Hard exudates - yellow lipid deposits from leaking vessels
• Soft exudates / cotton-wool spots - white fluffy patches from nerve fiber layer infarcts (microinfarcts)
• Flame hemorrhages (superficial) and dot-and-blot hemorrhages (deep)
• Venous beading - irregular caliber of retinal veins
• Macular edema - leakage into the macula → blurred central vision (most common cause of visual loss in NPDR)

• Triggered by retinal ischemia → release of VEGF → pathological neovascularization
• New vessels grow on the retinal surface and into the vitreous:
  • NVD (neovascularization of the disc)
  • NVE (neovascularization elsewhere)
• Complications: vitreous hemorrhage (sudden painless vision loss), tractional retinal detachment, rubeosis iridis (iris neovascularization) → neovascular glaucoma

2. Diabetic Nephropathy

1. Capillary basement membrane thickening - earliest change; begins ~2 years after T1D onset; best seen on electron microscopy; 30% increase in thickness by 5 years
2. Diffuse mesangial sclerosis - diffuse increase in mesangial matrix (PAS-positive deposits); reduces GFR; present in virtually all long-standing diabetics
3. Nodular glomerulosclerosis (Kimmelstiel-Wilson lesions) - pathognomonic for diabetes; ovoid PAS-positive nodules in periphery of glomeruli (mesangial nodules); associated with heavy proteinuria and progressive renal failure

• Renal arteriosclerosis (including efferent arteriole involvement - unique to diabetes; other diseases affect only afferent)
• Pyelonephritis (increased susceptibility to infection)
• Necrotizing renal papillitis (ischemic necrosis of renal papillae)

3. Diabetic Neuropathy

• Affects longest nerves first → "glove-and-stocking" distribution (feet and hands)
• Symptoms: burning, shooting, aching pain, paresthesias (tingling, numbness), "walking on hot coals" sensation
• Loss of: vibration sense, proprioception, light touch, pin-prick, temperature (ALL modalities)
• Loss of ankle jerk reflex (earliest sign)
• Risk of painless injuries → diabetic foot ulcers

• Cardiovascular: resting tachycardia, orthostatic hypotension, "silent ischemia" (40% of MI in diabetics go unrecognized - no chest pain!), sudden cardiac death risk
• GI: gastroparesis (delayed gastric emptying - nausea, vomiting, bloating, post-prandial hypoglycemia), diabetic diarrhea (especially nocturnal), constipation
• Genitourinary: erectile dysfunction (most common in men), neurogenic bladder (urinary retention → overflow incontinence), retrograde ejaculation
• Sudomotor: anhidrosis (reduced sweating), gustatory sweating (face sweats while eating)
• Hypoglycemia unawareness - impaired adrenergic response to hypoglycemia (no sweating, tremor, or palpitations as warning)

• Sudden onset of single nerve palsy
• CN III palsy (most classic diabetic cranial mononeuropathy) - ptosis + eye deviation → "pupil-sparing" CN III palsy (unlike aneurysm which is pupil-involving)
• CN VI, CN IV palsies (diplopia)
• Carpal tunnel syndrome (median nerve)
• Lateral femoral cutaneous nerve (meralgia paresthetica)
• Femoral neuropathy (diabetic amyotrophy) - severe thigh pain, weakness, atrophy

• Asymmetric proximal leg weakness + severe pain
• Thigh muscle wasting
• Self-limiting but can be debilitating

4. Diabetic Foot

• Peripheral neuropathy (loss of protective sensation)
• Peripheral vascular disease (ischemia)
• Excessive plantar pressure + repetitive trauma
• Impaired wound healing

MACROVASCULAR COMPLICATIONS

1. Coronary Artery Disease (CAD)

• Most common cause of death in T2D
• Diabetics have 2-4x the risk of CAD compared to non-diabetics
• "Silent ischemia" - absence of chest pain despite myocardial ischemia (due to cardiac autonomic neuropathy); very common in diabetics
• MI may present atypically: weakness, fatigue, confusion, pain in unusual locations
• Unrecognized MI rate: 40% in diabetics vs 25% in non-diabetics
• Higher risk of heart failure, cardiomyopathy (diabetic cardiomyopathy - independent of CAD)

2. Cerebrovascular Disease (Stroke)

• 2-4x increased risk of ischemic stroke
• Particularly lacunar infarcts (small vessel disease) - as discussed in the previous session
• Also increased risk of large artery atherothrombotic stroke
• Cerebral microangiopathy → cerebral vascular infarcts, small hemorrhages
• Contributes to vascular dementia

3. Peripheral Arterial Disease (PAD)

• Atherosclerosis of lower limb arteries (iliac, femoral, popliteal, tibial)
• Symptoms:
  • Intermittent claudication - cramping leg pain on walking, relieved by rest
  • Rest pain - severe burning pain at rest, especially at night, in feet
  • Critical limb ischemia - non-healing ulcers, gangrene
  • Absent or diminished peripheral pulses
  • Cold, pale/cyanotic limbs, hair loss over legs
• Leads to gangrene and amputation (macrovascular + microvascular + neuropathy combined)

Summary Diagram