Knee jerk ankle jerk planker jerk root value according to macloid

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Here's a quick answer while I search the textbooks:
Deep tendon reflexes and their root values (Macleod's):
  • Knee jerk (patellar reflex): L3, L4
  • Ankle jerk (Achilles reflex): S1, S2
  • Plantar reflex: L5, S1, S2
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deep tendon reflexes root values table knee jerk ankle jerk

This clinical photograph demonstrates the proper technique for eliciting the patellar tendon reflex (knee jerk) in a sitting position, incorporating the Jendrassik maneuver. The patient is seated on an examination table with legs hanging freely and knees flexed at a 90-degree angle, ensuring the feet do not touch the floor to allow for unobstructed lower leg extension. Simultaneously, the patient performs the Jendrassik maneuver by interlocking their fingers and attempting to pull their hands apart, a reinforcement technique designed to facilitate deep tendon reflexes (DTR) by reducing conscious inhibition and increasing upper motor neuron activation. The examiner, standing to the patient's side, is seen using a neurological reflex hammer to strike the patellar tendon just below the patella. This procedure tests the L3-L4 spinal segments and the femoral nerve. The image serves as an educational guide for neurological physical examination, highlighting proper patient positioning, the use of reinforcement maneuvers, and the anatomical striking point for DTR assessment.

This clinical photograph demonstrates the proper technique for eliciting the patellar tendon reflex (knee jerk) in a sitting position, incorporating the Jendrassik maneuver. The patient is seated on an examination table with legs hanging freely and knees flexed at a 90-degree angle, ensuring the feet do not touch the floor to allow for unobstructed lower leg extension. Simultaneously, the patient performs the Jendrassik maneuver by interlocking their fingers and attempting to pull their hands apart, a reinforcement technique designed to facilitate deep tendon reflexes (DTR) by reducing conscious inhibition and increasing upper motor neuron activation. The examiner, standing to the patient's side, is seen using a neurological reflex hammer to strike the patellar tendon just below the patella. This procedure tests the L3-L4 spinal segments and the femoral nerve. The image serves as an educational guide for neurological physical examination, highlighting proper patient positioning, the use of reinforcement maneuvers, and the anatomical striking point for DTR assessment.

A clinical photograph demonstrating the kneeling technique for eliciting the Achilles tendon reflex (ankle jerk), which tests the S1-S2 nerve roots and the tibial nerve. The patient is positioned kneeling on an examination table with their shins supported by the table surface and their feet hanging freely over the edge. This position allows for optimal relaxation of the gastrocnemius-soleus complex. The examiner is shown performing two simultaneous actions: using one hand to apply gentle passive dorsiflexion to the plantar surface of the foot to place the Achilles tendon under slight tension, and using a standard reflex hammer in the other hand to strike the tendon just above its insertion on the calcaneus. This procedural image illustrates a standard method in a neurological physical examination to assess deep tendon reflexes and identify possible upper or lower motor neuron pathology.

A clinical photograph demonstrating the kneeling technique for eliciting the Achilles tendon reflex (ankle jerk), which tests the S1-S2 nerve roots and the tibial nerve. The patient is positioned kneeling on an examination table with their shins supported by the table surface and their feet hanging freely over the edge. This position allows for optimal relaxation of the gastrocnemius-soleus complex. The examiner is shown performing two simultaneous actions: using one hand to apply gentle passive dorsiflexion to the plantar surface of the foot to place the Achilles tendon under slight tension, and using a standard reflex hammer in the other hand to strike the tendon just above its insertion on the calcaneus. This procedural image illustrates a standard method in a neurological physical examination to assess deep tendon reflexes and identify possible upper or lower motor neuron pathology.

This clinical photograph demonstrates the assessment of the patellar tendon reflex (knee-jerk) in a patient positioned supine. The patient's legs are arranged with the right leg crossed over the left, placing the uppermost knee in a flexed position that naturally stretches the quadriceps tendon. An examiner’s hand is visible, stabilizing the knee while using a reflex hammer with a circular rubber head to strike the patellar ligament just distal to the patella. This procedure is used to evaluate the L3-L4 spinal nerve roots and the integrity of the femoral nerve. The image illustrates a practical modification for eliciting deep tendon reflexes when a patient is in a semi-recumbent or supine position on an examination table, emphasizing proper limb positioning and strike location for clinical diagnostic purposes.

This clinical photograph demonstrates the assessment of the patellar tendon reflex (knee-jerk) in a patient positioned supine. The patient's legs are arranged with the right leg crossed over the left, placing the uppermost knee in a flexed position that naturally stretches the quadriceps tendon. An examiner’s hand is visible, stabilizing the knee while using a reflex hammer with a circular rubber head to strike the patellar ligament just distal to the patella. This procedure is used to evaluate the L3-L4 spinal nerve roots and the integrity of the femoral nerve. The image illustrates a practical modification for eliciting deep tendon reflexes when a patient is in a semi-recumbent or supine position on an examination table, emphasizing proper limb positioning and strike location for clinical diagnostic purposes.

Here is the complete answer on reflex root values, as given by Macleod's Clinical Examination and corroborated by multiple authoritative neurology and surgery textbooks:

Deep Tendon Reflexes - Root Values (Macleod's)

ReflexRoot ValueNotes
Knee Jerk (Patellar reflex)L3, L4 (mainly L4)Tests femoral nerve; knee extension arc
Ankle Jerk (Achilles reflex)S1 (S1-S2)Tests tibial nerve; plantar flexion arc
Plantar reflexL5, S1, S2Normal = flexion (downgoing); Abnormal upgoing = Babinski sign (UMN lesion)

Additional Lower Limb Reflexes for Context

ReflexRoot Value
Cremasteric reflexL1-L2
Medial hamstringL5
BulbocavernosusS2-S4
Anal winkS3-S4

Key Points

  • Knee jerk (L3-L4, mainly L4): Loss indicates L3/L4 root lesion or femoral nerve injury. Seen in L4 disc prolapse.
  • Ankle jerk (S1): Loss is the hallmark of S1 radiculopathy (e.g., L5-S1 disc herniation). Also lost in peripheral neuropathy (often symmetric).
  • Plantar reflex (L5-S2): A flexor (downgoing) response is normal. A Babinski sign (upgoing great toe + fan of other toes) indicates upper motor neuron damage - never a root value issue per se, but the arc runs through L5-S2 cord segments.

Memory Aid

"1, 2 buckle my shoe" (ankle = S1-2); "3, 4 knock at the door" (knee = L3-4)
Knee jerk (patellar reflex) technique showing L3-L4 testing
Ankle jerk (Achilles reflex) kneeling technique showing S1-S2 testing
Sources: Sabiston Textbook of Surgery (Neurologic Examination section), Rheumatology 2-Volume Set (Deep Tendon Reflexes section), Neuroanatomy through Clinical Cases 3e (Cauda Equina / Lumbosacral Radiculopathy table), and multiple neurology references confirming the same root values.

Knee jerk ankle jerk planter reflex exgarrated and deminish r cause

Searching the medical library for exaggerated and diminished reflex causes.
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UMN LMN reflex comparison upper lower motor neuron signs diagram

A medical schematic diagram illustrating the neuroanatomical pathways of upper motor neurons (UMN) and lower motor neurons (LMN) and their selective involvement in Amyotrophic Lateral Sclerosis (ALS) variants. The diagram features a lateral view of the human brain, a coronal section of the brain, and transverse sections of the spinal cord (cervical and lumbar levels). Two primary tracts are highlighted: the corticobulbar (CB) tract, represented by green solid circles (UMN) and open circles (LMN), and the corticospinal (CS) tract, represented by blue solid circles (UMN) and open circles (LMN). Solid circles represent UMN cell bodies in the motor cortex, while open circles denote LMNs in the brainstem (bulbar) and spinal cord. Colored vertical tick marks inside these circles indicate specific disease phenotypes: red for classic ALS (CS & CB UMN and LMN), black for Primary Lateral Sclerosis (PLS, UMN only), and yellow for Progressive Muscular Atrophy (PMA, LMN only). Other variants shown include Pseudobulbar palsy (CB UMN), Flail arm, and Flail leg (specific CS LMN segments). This illustration serves as an educational tool for differentiating motor neuron disease phenotypes based on the anatomical site of degeneration.

A medical schematic diagram illustrating the neuroanatomical pathways of upper motor neurons (UMN) and lower motor neurons (LMN) and their selective involvement in Amyotrophic Lateral Sclerosis (ALS) variants. The diagram features a lateral view of the human brain, a coronal section of the brain, and transverse sections of the spinal cord (cervical and lumbar levels). Two primary tracts are highlighted: the corticobulbar (CB) tract, represented by green solid circles (UMN) and open circles (LMN), and the corticospinal (CS) tract, represented by blue solid circles (UMN) and open circles (LMN). Solid circles represent UMN cell bodies in the motor cortex, while open circles denote LMNs in the brainstem (bulbar) and spinal cord. Colored vertical tick marks inside these circles indicate specific disease phenotypes: red for classic ALS (CS & CB UMN and LMN), black for Primary Lateral Sclerosis (PLS, UMN only), and yellow for Progressive Muscular Atrophy (PMA, LMN only). Other variants shown include Pseudobulbar palsy (CB UMN), Flail arm, and Flail leg (specific CS LMN segments). This illustration serves as an educational tool for differentiating motor neuron disease phenotypes based on the anatomical site of degeneration.

An anatomical illustration and 3D artistic model depicting a comparative visualization of the motor homunculus. The larger, flesh-colored figure represents the Upper Motor Neuron (UMN) homunculus, traditionally based on the cortical mapping of the primary motor cortex. It features massive hands, large feet, and prominent facial structures, illustrating the high density of cortical neurons dedicated to fine motor control in these regions. Juxtaposed to it is a smaller, blue-colored figure representing the Lower Motor Neuron (LMN) homunculus. The LMN homunculus is scaled relative to the UMN counterpart, with its bodily proportions determined by alpha motor neuron densities within the spinal cord and brainstem. This comparative diagram highlights the differences in somatotopic representation between the cerebral motor system and the final common pathway. The visual serves as a neuroanatomical educational tool to demonstrate how motor innervation complexity varies across different levels of the central nervous system, emphasizing the disproportionate neural representation of the hands and face in human motor control.

An anatomical illustration and 3D artistic model depicting a comparative visualization of the motor homunculus. The larger, flesh-colored figure represents the Upper Motor Neuron (UMN) homunculus, traditionally based on the cortical mapping of the primary motor cortex. It features massive hands, large feet, and prominent facial structures, illustrating the high density of cortical neurons dedicated to fine motor control in these regions. Juxtaposed to it is a smaller, blue-colored figure representing the Lower Motor Neuron (LMN) homunculus. The LMN homunculus is scaled relative to the UMN counterpart, with its bodily proportions determined by alpha motor neuron densities within the spinal cord and brainstem. This comparative diagram highlights the differences in somatotopic representation between the cerebral motor system and the final common pathway. The visual serves as a neuroanatomical educational tool to demonstrate how motor innervation complexity varies across different levels of the central nervous system, emphasizing the disproportionate neural representation of the hands and face in human motor control.

Here is a complete, organized breakdown of causes of exaggerated and diminished knee jerk, ankle jerk, and plantar reflexes:

Grading of Deep Tendon Reflexes (DTR)

GradeMeaning
0Absent
1+Hypoactive (diminished)
2+Normal (brisk)
3+Hyperactive, no clonus
4+Hyperactive with mild clonus
5+Hyperactive with sustained clonus
(Ganong's Review of Medical Physiology, 26e)

1. KNEE JERK (L3-L4, Patellar Reflex)

Exaggerated (Hyperreflexia) - Causes

These indicate Upper Motor Neuron (UMN) lesion - damage to corticospinal tract above L3-L4:
CauseMechanism
Stroke (cerebrovascular accident)Corticospinal tract interruption
Multiple sclerosisDemyelination of UMN pathways
Cervical/thoracic myelopathyCord compression above L3
Spinal cord injury (above L3)Loss of descending inhibition
Brain tumorCortical/subcortical UMN involvement
Amyotrophic lateral sclerosis (ALS)Both UMN + LMN involved
Cerebral palsyUMN lesion
HyperthyroidismIncreased neuromuscular excitability
Anxiety / tensionReduced cortical inhibition
TetanusLoss of inhibitory interneurons

Diminished / Absent - Causes

These indicate Lower Motor Neuron (LMN) lesion anywhere in the reflex arc (spindle → Ia afferent → L3-L4 anterior horn → femoral nerve → quadriceps):
CauseMechanism
L3/L4 disc prolapseRoot compression
Diabetic neuropathyIa afferent fiber damage
Alcoholic neuropathyPeripheral nerve damage
Guillain-Barré syndromeAcute demyelinating polyneuropathy
Femoral nerve injuryLMN arc disruption
Tabes dorsalis (syphilis)Posterior root/dorsal column damage
HypothyroidismSlow relaxation phase ("hung-up reflex")
Hypokalemia / hypomagnesemiaNeuromuscular junction dysfunction
MyopathyMuscle disease (quadriceps wasting)
Shock/coma (acute)Generalized depression of CNS
AgingPhysiologic reduction in elderly

2. ANKLE JERK (S1, Achilles Reflex)

Exaggerated - Causes

UMN lesion above S1 (same principle as knee jerk):
  • Stroke, spinal cord lesion (above S1), MS, myelopathy, ALS
  • Hyperthyroidism - classically causes brisk reflexes with fast relaxation phase
  • Anxiety, clonus present in severe UMN lesions

Diminished / Absent - Causes

This is the most commonly lost reflex in clinical practice:
CauseNotes
S1 radiculopathy (L5-S1 disc)Most common cause of absent ankle jerk
Diabetic peripheral neuropathyFirst reflex to be lost; distal > proximal
Alcoholic neuropathyLength-dependent axonopathy
Guillain-Barré syndromeEarly bilateral absent ankle jerks
Charcot-Marie-Tooth diseaseHereditary neuropathy
Hypothyroidism"Hung-up" or absent ankle jerk - classic sign
Aging (normal)Achilles reflex often absent in elderly
Sciatic nerve injuryLMN arc at sciatic/tibial level
Vitamin B12 deficiencySubacute combined degeneration
Tabes dorsalisPosterior column + root damage
Carcinomatous neuropathyParaneoplastic
Clinical pearl: Absent ankle jerk + upgoing plantars = combined UMN + LMN lesion → think subacute combined degeneration of cord (B12 deficiency) or motor neuron disease (ALS)

3. PLANTAR REFLEX (L5-S1-S2)

Normal Response

Stroking the lateral sole → flexion (downgoing) of all toes = flexor plantar response (normal)

Exaggerated / Abnormal = BABINSKI SIGN

Extension (upgoing) of great toe + fanning of other toes = upper motor neuron lesion
Cause of Positive BabinskiNotes
StrokeMost common cause
Spinal cord compression/traumaAny level above S1
Multiple sclerosisDemyelination of CST
Meningitis/encephalitisAcute CNS inflammation
Brain tumorCST involvement
Todd's paralysis (post-seizure)Transient Babinski
Hypoglycemic comaMetabolic UMN depression
Deep sleep / anaesthesiaNormal in unconscious state
Infants < 18 monthsNormal finding - corticospinal tract not yet myelinated

Diminished / Absent Plantar Response

  • Peripheral neuropathy - sensory afferents of sole damaged (cannot elicit the reflex)
  • S1-S2 root lesion - efferent arc disrupted
  • Heavy callus on foot - cannot elicit stimulus

Summary Table

ReflexExaggerated (UMN)Diminished (LMN/Peripheral)
Knee jerkStroke, MS, myelopathy, hyperthyroidism, ALSL3-L4 disc, DM neuropathy, GBS, femoral nerve lesion, hypothyroidism
Ankle jerkStroke, myelopathy, MS, hyperthyroidismS1 radiculopathy, DM neuropathy, hypothyroidism, GBS, B12 deficiency, aging
PlantarPositive Babinski = stroke, MS, cord injury, ALS, encephalitis, post-ictalAbsent = peripheral neuropathy, S1-S2 root lesion

Key Concept: A hyperreflexia with positive Babinski = UMN lesion (brain or cord). A hyporeflexia/areflexia = LMN lesion, peripheral nerve, or neuromuscular junction problem. The distinction between UMN and LMN is the single most important localizing principle in neurology.
(Sources: Ganong's Review of Medical Physiology 26e; Rosen's Emergency Medicine; Bradley and Daroff's Neurology in Clinical Practice; Sabiston Textbook of Surgery)

Touch pain vibration joint position eigula loss hoi kokhn

The question is asking: "When does loss of touch, pain, vibration, and joint position sense occur?" - i.e., which sensory modalities are lost in which conditions/lesions.
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sensory pathways spinal cord dorsal column spinothalamic tract diagram cross section

Anatomical diagram of a spinal cord cross-section illustrating the pathway of the ventral spinothalamic tract (VST). The illustration depicts the central H-shaped gray matter and surrounding white matter. Key structures labeled include Rexed laminae VI, VII, and VIII in the dorsal and intermediate horns of the gray matter. A black arrow indicates the origin of secondary sensory neurons within these deep laminae. A white arrow tracks the decussation (crossing over) of these nerve fibers through the anterior white commissure to the contralateral side. The fibers terminate in the ventral white column, labeled as the 'VST' tract. This diagram serves as a neuroanatomical representation of the ascending somatosensory pathway for crude touch and pressure, highlighting its origin in non-opioid-rich Rexed layers compared to the lateral spinothalamic tract.

Anatomical diagram of a spinal cord cross-section illustrating the pathway of the ventral spinothalamic tract (VST). The illustration depicts the central H-shaped gray matter and surrounding white matter. Key structures labeled include Rexed laminae VI, VII, and VIII in the dorsal and intermediate horns of the gray matter. A black arrow indicates the origin of secondary sensory neurons within these deep laminae. A white arrow tracks the decussation (crossing over) of these nerve fibers through the anterior white commissure to the contralateral side. The fibers terminate in the ventral white column, labeled as the 'VST' tract. This diagram serves as a neuroanatomical representation of the ascending somatosensory pathway for crude touch and pressure, highlighting its origin in non-opioid-rich Rexed layers compared to the lateral spinothalamic tract.

Educational neuroanatomical schematic of a rodent spinal cord cross-section, divided into two panels. Panel A illustrates the distribution and connectivity of spinal interneurons. Blue circles represent dorsally-derived interneurons (e.g., dI3, dI4) located in the dorsal horn, while red circles represent ventrally-derived interneurons (e.g., V0, V1, V2a, V3) in the ventral horn and intermediate zone. Black lines depict axonal projections from these interneuron populations synapsing onto motoneurons (MN). Panel B provides a detailed topographical map of white matter tracts. Ascending sensory pathways include the gracile fasciculus and postsynaptic dorsal column pathway medially, with the spinothalamic and spinocerebellar tracts located laterally. Descending motor pathways include the dorsal corticospinal tract, rubrospinal tract, and various reticulospinal and vestibulospinal tracts distributed throughout the ventral and lateral funiculi. This diagram serves as a foundational tool for understanding spinal circuit organization, sensorimotor integration, and neuroanatomical localization within the central nervous system.

Educational neuroanatomical schematic of a rodent spinal cord cross-section, divided into two panels. Panel A illustrates the distribution and connectivity of spinal interneurons. Blue circles represent dorsally-derived interneurons (e.g., dI3, dI4) located in the dorsal horn, while red circles represent ventrally-derived interneurons (e.g., V0, V1, V2a, V3) in the ventral horn and intermediate zone. Black lines depict axonal projections from these interneuron populations synapsing onto motoneurons (MN). Panel B provides a detailed topographical map of white matter tracts. Ascending sensory pathways include the gracile fasciculus and postsynaptic dorsal column pathway medially, with the spinothalamic and spinocerebellar tracts located laterally. Descending motor pathways include the dorsal corticospinal tract, rubrospinal tract, and various reticulospinal and vestibulospinal tracts distributed throughout the ventral and lateral funiculi. This diagram serves as a foundational tool for understanding spinal circuit organization, sensorimotor integration, and neuroanatomical localization within the central nervous system.

This medical anatomical diagram illustrates a cross-section of the spinal cord (medulla oblongata level, approximately 18 mm below the obex), specifically focusing on the neuroanatomical structures targeted during a trigeminal nucleotomy. The diagram highlights both white matter tracts and gray matter nuclei. In the posterior column, the Fasciculus Gracilis (FG) is medially positioned, while the Fasciculus Cuneatus (FC) is lateral to it. The lateral white matter contains the Lateral Corticospinal Tract (LCST), Dorsal Spinocerebellar Tract (DSCT), and Ventral Spinocerebellar Tract (VSCT). On the right side of the diagram, a surgical probe is shown penetrating the Spinal Trigeminal Tract (STT/STrigT) to target the Spinal Trigeminal Nucleus (STN), specifically indicating the Gelatinosa Portion (GP) and the Magnocellular Portion (MC). Other notable structures include the Rubrospinal Tract (RST) and the Lateral Spinothalamic Tract (LSTT). This illustration is designed for neurosurgical education, demonstrating the spatial relationships necessary for selective destruction of pain-transmitting nuclei in the brainstem and upper cervical spinal cord.

This medical anatomical diagram illustrates a cross-section of the spinal cord (medulla oblongata level, approximately 18 mm below the obex), specifically focusing on the neuroanatomical structures targeted during a trigeminal nucleotomy. The diagram highlights both white matter tracts and gray matter nuclei. In the posterior column, the Fasciculus Gracilis (FG) is medially positioned, while the Fasciculus Cuneatus (FC) is lateral to it. The lateral white matter contains the Lateral Corticospinal Tract (LCST), Dorsal Spinocerebellar Tract (DSCT), and Ventral Spinocerebellar Tract (VSCT). On the right side of the diagram, a surgical probe is shown penetrating the Spinal Trigeminal Tract (STT/STrigT) to target the Spinal Trigeminal Nucleus (STN), specifically indicating the Gelatinosa Portion (GP) and the Magnocellular Portion (MC). Other notable structures include the Rubrospinal Tract (RST) and the Lateral Spinothalamic Tract (LSTT). This illustration is designed for neurosurgical education, demonstrating the spatial relationships necessary for selective destruction of pain-transmitting nuclei in the brainstem and upper cervical spinal cord.

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Excellent textbook data retrieved. Here is the complete, organized answer:

Sensory Modalities - When Each Is Lost (Anatomical Basis)

First: The Two Key Sensory Pathways

Understanding which pathway carries which sensation is the foundation of everything:
PathwaySensation CarriedRoute
Dorsal Column - Medial Lemniscus (DCML)Fine touch, Vibration, Joint position sense (proprioception), 2-point discriminationEnters spinal cord → goes UP ipsilateral dorsal column → crosses at MEDULLA
Lateral Spinothalamic Tract (STT)Pain, Temperature, Crude touchEnters spinal cord → crosses within 2-3 segments in anterior white commissure → goes UP contralateral STT

Condition-wise Sensory Loss Pattern

1. DORSAL COLUMN LESION (Posterior column)

Lost: Vibration + Joint position sense + Fine touch Preserved: Pain + Temperature
DiseaseNotes
Tabes dorsalis (tertiary syphilis)Classic posterior column destruction
Subacute combined degeneration (Vit B12 deficiency)Posterior + lateral columns both affected
Multiple sclerosisPlaque in dorsal column
Friedreich's ataxiaSpinocerebellar + dorsal columns
Posterior cord syndrome (spinal injury)Dorsal column spared or damaged specifically
Clinical sign: Romberg's sign positive (falls on closing eyes - proprioception lost)

2. SPINOTHALAMIC TRACT (LATERAL) LESION

Lost: Pain + Temperature (contralateral to lesion) Preserved: Vibration + Joint position
DiseaseNotes
SyringomyeliaCentral cavity destroys crossing fibers → cape-like suspended sensory loss of pain + temperature in arms/shoulders; touch/vibration preserved
Anterior Spinal Artery SyndromeInfarcts anterior cord → loss of pain + temperature BELOW lesion; vibration + proprioception PRESERVED
Central cord syndrome (hyperextension injury)Crossing fibers damaged → dissociated loss; arms > legs
Lateral medullary syndrome (Wallenberg's)Contralateral body pain + temperature loss

3. COMPLETE UNILATERAL CORD LESION - BROWN-SEQUARD SYNDROME

(Hemisection of spinal cord)
SideModality Lost
Ipsilateral (same side as lesion)Vibration + Joint position (dorsal column) + Motor (UMN)
Contralateral (opposite side)Pain + Temperature (STT crosses before ascending)
Causes: Penetrating injury, MS, tumor, disc prolapse

4. ALL SENSORY MODALITIES LOST (Complete cord / peripheral lesion)

ConditionPattern
Complete spinal cord transectionALL sensation lost below level (both pathways cut)
Peripheral neuropathy (DM, alcohol, GBS)Loss of all modalities, distal > proximal, "glove and stocking"
Thalamic infarctionContralateral loss of all sensory modalities
Cortical lesionContralateral loss, especially discriminative touch + proprioception

5. ONLY TOUCH LOST (Rare)

  • Anterior spinothalamic tract lesion - crude touch alone
  • Cortical parietal lobe lesion - fine/discriminative touch, 2-point discrimination, graphesthesia lost while pain may be preserved

Master Summary Table

ModalityPathwayLost In
Fine touch, 2-point discriminationDorsal columnB12 deficiency, tabes dorsalis, MS, parietal cortex lesion
VibrationDorsal columnB12 deficiency, tabes dorsalis, Friedreich's ataxia, MS, peripheral neuropathy (early loss distally)
Joint position (proprioception)Dorsal columnSame as vibration; also causes sensory ataxia + Romberg positive
PainSpinothalamic (crosses early)Syringomyelia (dissociated), anterior spinal artery syndrome, Brown-Sequard (contralateral)
TemperatureSpinothalamic (crosses early)Same as pain - always lost together with pain
Crude touchAnterior spinothalamicRarely lost in isolation; lost in complete cord/peripheral lesions

The "Dissociated Sensory Loss" Concept (High-Yield)

Dissociated sensory loss = one type of sensation lost, another preserved at the SAME level
TypeWhat's LostWhat's PreservedClassic Disease
Spinothalamic lossPain + TemperatureVibration + PositionSyringomyelia, Anterior spinal artery syndrome
Dorsal column lossVibration + PositionPain + TemperatureTabes dorsalis, B12 deficiency
Brown-SequardIpsilateral vibration/position + Contralateral pain/tempBoth sides partially preservedPenetrating cord injury

(Sources: Bradley and Daroff's Neurology in Clinical Practice - Spinal Sensory Lesions; Goldman-Cecil Medicine - Syringomyelia; Localization in Clinical Neurology 8e - Spinal Cord Syndromes)
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