Download upper motor neuron hemiplegia-paraplegia

UPPER MOTOR NEURON
HEMIPLEGIA-PARAPLEGIA
DR NASIR FAROOQ BUTT
ASSISTANT PROFESSOR
DEPARTMENT OF MEDICINE
KING EDWARD MEDICAL UNIVERSITY
MAYO HOSPITAL LAHORE
• UPPER MOTOR NEURONS (UMN) start from
cerebral cortex, passes through internal capsule,
corticospinal tracts, and ends at cranial nerve nuclei
in brain stem or anterior horn cells of spinal cord at
different levels. The axons of upper motor neurons
are contained within the pyramidal system, which is
composed of the corticospinal (pyramidal) and
corticobulbar tracts.
• LOWER MOTOR NEURONS (LMN) start from nuclei
of cranial nerves or anterior horn cells of spinal cord,
extend through cranial /spinal nerves and ends at
motor end plate of concerned muscle.
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UPPER MOTOR NEURONS LESION
(UMNL)
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Pyramidal Drift Of An Upper
Limb
Normally, the outstretched upper limbs are
held symmetrically, when the eyes are closed.
With a pyramidal lesion, when both upper
limbs are held outstretched, palms
uppermost, the affected limb drifts
downwards and medially. The forearm tends
to pronate and the fingers flex slightly. This
sign is often first to emerge, sometimes
before weakness and/or reflex changes
become apparent.
Pyramidal Drift Of An Upper
Limb
Weakness And Loss Of Skilled
Movement
 A unilateral pyramidal lesion above the
decussation in the medulla causes weakness of
the opposite limbs.
 When acute and complete, this weakness will be
immediate and total, a hemiplegia, e.g.
following an internal capsule infarct.
 With slowly progressive lesions (e.g. a
hemisphere glioma) a characteristic pattern of
weakness emerges – a hemiparesis.
 There is also loss of skilled movement – fine
finger and toe control diminishes.
Changes In Tone And Tendon
Reflexes
 An acute lesion of one pyramidal tract (e.g.
internal capsule stroke) causes initially FLACCID
paralysis with loss of tendon reflexes.
 Increase in tone follows, usually within several
days due to loss of inhibitory effects of the
corticospinal pathways and an increase in
spinal reflex activity.
 SPASTICITY is characterized by sudden
changing resistance to passive movement – the
clasp-knife effect.
 Relevant TENDON REFLEXES become
exaggerated;
 CLONUS may emerge.
Changes In Superficial Reflexes
Abdominal (and cremasteric) reflexes are
abolished on the side affected.
The Babinski sign.
Patterns of UMN disorders
There are three main patterns:
 HEMIPARESIS means weakness of the limbs on
one side; it is usually caused by a lesion in
the brain and occasionally in the cord.
 PARAPARESIS means weakness of both lower
limbs and usually diagnostic of a cord lesion;
bilateral brain lesions occasionally cause
paraparesis.
 TETRAPARESIS (syn. quadriparesis) means
weakness of four limbs.
Extrapyramidal system
The extrapyramidal system is a general term for
BASAL GANGLIA motor systems, i.e. corpus striatum (caudate
nucleus + globus pallidus + putamen), subthalamic nucleus,
substantia nigra and parts of the thalamus. In basal ganglia/
extrapyramidal disorders, two features (either or both)
become apparent, in limbs and axial muscles:
 Reduction in speed (bradykinesia, meaning slow
movement) or akinesia (no movement), with muscle
rigidity
 Involuntary movements (e.g. tremor, chorea,
hemiballismus, athetosis, dystonia).
Extrapyramidal system
• Extrapyramidal disorders are classified broadly into:
Akinetic-rigid Syndromes where poverty
of movement predominates
Dyskinesias where there are involuntary
movements.
• The most common extrapyramidal disorder is
Parkinson’s disease.
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Case Scenario
• An 83-year-old right-handed woman was eating
dinner when she suddenly slumped to the right and
her speech became slurred and nonfluent. Her
vascular risk factors were hypertension and
dyslipidemia, and the only other past medical
history of interest was long-term hypothyroidism
and a curative mastectomy for breast cancer. The
patient was on two antihypertensive medications
and a statin, and was not receiving any antiplatelet
medication. Her husband immediately called the
emergency medical services.
Case Scenario
On Examination Pulse is 84/min (regular), BP:
180/105 mm Hg.
Angle of mouth is deviated towards left (UMN type
Right 7th CN)
Tone is decreased in right upper and lower limb,
Power is 2/5 in right right upper and lower limb,
Reflexex are absent in right right upper and lower
limb.
Right Planter is upgoing.
Tone, power, reflexes are normal on left side with
downgoing planter
What is your Diagnosis????
STROKE
This patient has had STROKE causing
Right sided uncrossed Hemiplegia with
UMN type Facial Nerve Palsy which can
be caused by a vascular event such as
thrombosis, embolism or hemorrhage or
by neaplasm of brain (aetiology). The
patient is limited by hemiplegia
(functional status)
Stroke
DEFINITION: Stroke is defined as a
syndrome of rapid onset of cerebral
deficit (usually focal) lasting >24 h or
leading to death, with no cause
apparent other than a vascular one.
Stroke
Ischaemic stroke/infarction (80%)
 Thrombotic
 Cardio-embolic
 Large artery stenosis
 Small vessel disease
 Hypoperfusion
Haemorrhagic stroke (17%)
 Intracerebral hemorrhage (12%)
 Subarachnoid hemorrhage (5%)
Other (3%), e.g. arterial dissection, venous sinus
thrombosis, vasculitis
Types of Stroke
Depending upon the rate of developing and reversibility, stroke can be
of following types:
 Transient Ischemic Attack (TIA): means a brief episode of
neurological dysfunction due to temporary focal cerebral
or retinal ischemia without infarction, e.g. a weak limb,
aphasia or loss of vision, usually lasting seconds or
minutes with complete recovery.
 Stroke-in-Evolution: If neurological deficit increases by
step wise progression or there is slow uninterrupted
progression, it is called stroke-in-evolution. It may take 12 weeks to complete
 Complete Stroke: It means complete hemiplegia
 RIND (Reversible Ischemic Neurological Deficit): It is a term that is
not widely used anymore. It means a stroke that the patient was
able to fully recover from within a few weeks.
Types of Stroke
Depending upon the blood supply of affected area of
brain, stroke can be of following types:
 ANTERIOR CIRCULATION STROKE:
Carotid system
 POSTERIOR CIRCULATION STROKE:
Vertebrobasilar system
Risk Factor For Ischemic Stroke
 Hypertension
 Diabetes
 Smoking
 Lifestyle
 Alcohol
 High cholesterol
 Atrial fibrillation
 Obesity
 Severe carotid stenosis
 Sleep apnoea
Rarer Causes Of Stroke
 Hyperviscosity states.
Thrombocythaemia,
Polycythaemia
Thrombophilia
 Anti-cardiolipin and lupus anticoagulant
antibodies
 oral contraceptive.
 Migraine
 Vasculitis
Systemic lupus erythematosus (SLE),
Polyarteritis
Giant cell arteritis
Granulomatous CNS angiitis
Rarer Causes Of Stroke
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Amyloidosis.
Hyperhomocysteinaemia
Neurosyphilis
Mitochondrial disease
Drugs
 Sympathomimetic drugs
 cocaine
 Vasoconstrictors
 neuroleptics
• CADASIL (cerebral dominant arteriopathy with
subcortical infarcts and leucoencephalopathy)
Clinical Features of Stroke
 SYMPTOMS:
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Weakness of one half of body
Onset – Sudden, can be gradual
Headache, vomiting, fits
Unconciousness
Past H/O TIAs
H/O smooking, HTN, DM or IHD
Family H/O Stroke
Clinical Features of Stroke
 SIGNS:
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PULSE: Irregular (At. Fib), Slow (Raised ICP)
BP: High
Unconciouness
Pupils: Small or Dilated
EYES: Devited towards on side (conjugate gaze)
Cranial Nerves may be involved
Dysphasia, Dysarthria
Initially limbs may be flaccid with absent reflexes
(Spinal Shock). This may persist for days, weeks or
months and then Classical UMNL signs develop
Clinical Features of Stroke
 SIGNS:
Hemiplegic weakness of upper limb affects the
shoulder abductor, elbow extensors, wrist and finger
extensors and small musles of hand
Hemiplegic weakness of lower limb affects hip
flexors, knee flexors and dorsiflexors and evertors of
the foot
Clinical Features of Stroke
 SIGNS:
• Signs of meningial irritation (SOMI) – Subarachnoid
Hemorrhages
• Fundoscopy: Diabetic or Hypertensive Retinopathy
• Carotid Pulsation: weak, bruit
• CVS Exam: Murmur eg Mitral stenosis
• Homonymous hemianopia and sensory inattention
• Speech defects
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Amaurosis fugax
• Refers to a transient loss of vision in one or
both eyes due to embolism in retinal artery.
• This is a feature of TIA in carotid circulation
ISCHEMIC STROKE
Cerebral Thrombosis:
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Occurs when patient is asleep
Atherosclerotic narrowing of blood vessel
Middle cerebral art is commonly involved
Patient usually remain conscious
HTN is a major risk factor
Clinical Features:
Pt can not move one half of body
Dysphasia
Uncrossed hemiplegia
High BP
Carotid Bruit
ISCHEMIC STROKE
Cerebral Embolism:
 Sudden onset
 Past history of TIAs
 Source of Embolism
 Carotid artery atheroma (weak carotid pulse,bruit)
 Atrial Fibrillation or other arrythmias
 Recent Myocardial Infarction
 Valvular Heart Disease
 Infective Endocarditis
 Clinical Features:
 Sudden loss of power in one half of body
 Conciouness may be lost
 Dysphasia
 Uncrossed hemiplegia
 Irregular Pulse
 Signs of valvular heart disease
 Carotid Bruit
HEMORRHAGIC STROKE
Primary Intracerebral Hemorrhage:
 H/O HTN
 Internal capsule is most common site. Other sites:
subcortical white matter, pons, and cerebellum.
 Occurs when pt is engaged in some activity
 Causes: HTN, Saccular Aneurysm, AV Malformation,
Bleeding Disorders
 Clinical Features:
Sudden loss of power in one half of body
Headache, vomiting and loss of Conciouness
Uncrossed hemiplegia
Fundoscopy: Papilledema
HEMORRHAGIC STROKE
Subarachnoid Hemorrhage:
 Primary: Bleeding occurs directly into subarachnoid space.
 Causes: Saccular Aneurysm, AV Malformation, Bleeding
Disorders, Vasculitis
 Clinical Features:
Sudden onset of severe Headache with or without
vomiting
SOMI are present
Focal neurological signs
Fundoscopy: Subhyloid hemorrhage, Papilledema
Secondary: Extension of intracerebral hemorrhage into
subarachnoid space
SPACE OCCUPYING LESION
Lesion which occupy the cranial cavity and displace or
destroy existing structures
Causes: Tumour, Abscess, Hematoma, Tuberculomas
Symptoms:
H/O gradual onset of weakness developing over weeks to months.
Headache and vomiting
There may be H/O trauma (Hematoma)
H/O waxing and waning of concious level (Subdural Hematoma)
H/O fever and ear discharge suggest an abscess.
Signs:
In addition to motor deficit, following signs may be present:
Bradycardia
Fundoscopy……Papilledema
Investigations:
CT scan (with contrast), MRI
Localization of Lesion
UNCROSSED HEMIPLEGIA:
Cranial nerves involvement and hemiplegia are on the same side
Lesion is above brainstem on the side opposite to the
hemiplegia
CROSSED HEMIPLEGIA:
Cranial nerves are involved on one side and hemiplegia is on the
other side
Lesion is in brainstem on the side of cranial nerve involvement.
HEMIPLEGIA WITHOUT CRANIAL NERVES
INVOLVEMENT:
Lesion is in spinal cord above C5 on the side of paralysis.
Localization of Lesion
UNCROSSED HEMIPLEGIA:
Lesion can be in Motor cortex, Corona Radiata or Internal
Capsule
Motor cortex:
Specific manifestation due to lesion of various lobes:
 Parietal Lobe
 Temporal Lobe
 Occipital Lobe
 Frontal Lobe
Localization of Lesion
PARIETAL LOBE:
Sensory cortex (Precentral Gyrus) demage only affects
special sensory functions
• Loss of cortical sensations:
 Two point discrimination
 Astereogonosis (inability to identify common objects by
palpation with one hand while senses are intact)
• Homonymous lower quadrantanopia
• Apraxia (inability to perform a learned act in the absence of
significant motor weakness.
• Additional Features of Dominant Hemisphere
 Gerstmann’s synd: Inability to calculate, write, distinguish
between right and left, to recognize different fingers.
 Alexia (inability to read), Bimanual astereognosis, Sensory
dysphasia
Localization of Lesion
PARIETAL LOBE:
Additional Features of Non- Dominant Hemisphere
 Sensory inattention (when both side are touched
separately patient can recognize them, but when they
are touched simultaneously, side opposite to affected
parietal lobe is ignored)
 Indifference to illness
 Anosognosia (pt is unaware of paralysis)
 Autopagnosia (pt ignores paralyzed body)
 Spatial disorientation ( Pt is unable to find his way
around)
Localization of Lesion
TEMPORAL LOBE:
Auditory or Olfactory hallucination
Auditory or Visual hallucination
Homonymous upper quadrantanopia of opposite side
Deja vu phenomenon (feeling of undue familiarity with
surroundings)
• Automatism (lip smacking, swallowing, walking
aimlessly or unconscious performance of highly skilled
activity like driving a car)
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OCCIPITAL LOBE:
• Visual hallucination
• Homonymous hemianopia of opposite side
Localization of Lesion
PRE-FRONTAL LOBE :
• Lack of initiative and concentration
• Lack of concern of consequences of any action
• Micturition disturbance
• Grasp Reflex is +ve
PRECENTRAL GYRUS (FRONTAL LOBE):
• Weakness of of opposite half of the body
• Jacksonian fits
• Expressive, motor or non-fluent dysphasia if lesion is
in the dominant hemisphere.
Localization of Lesion
UNCROSSED HEMIPLEGIA:
CORONA RADIATA:
Although Weakness is more marked in one limb, whole half is
involved to some extent
INTERNAL CAPSULE:
Motor and sensory fibere are very closely packed…so lesion cause
 Dense complete hemiplegia
 Facial nerve palsy of same side
 Cortical sensory loss and hemianopia may occur
Localization of Lesion
CROSSED HEMIPLEGIA:
Midbrain:
 3rd /4th CN are involved on one side and hemiplegia of
opposite side
Pons:
 5th, 6th, 7th and 8th CN nuclei are present in pons.
 One or more of these CNs are paralyzed on one side and
hemiplegia is on the other side.
 Pupils are pinpoint but reactive to light
 Hyperpyrexia may be present
Medulla Oblongata:
 9th, 10th, 11th and 12th CN nuclei are present in medulla.
 One or more of these CNs are paralyzed on one side and
hemiplegia is on the other side.
Localization of Lesion
SPINAL CORD.
Brown-Sequard syndrome (BSS) is a rare
neurological condition characterized by a lesion
in the spinal cord which results in weakness or
paralysis (hemiparaplegia) on one side of the
body and a loss of sensation (hemianesthesia) on
the opposite side.
Causes:
• Trauma
• Non-traumatic: Tumor (primary or metastatic),
Multiple sclerosis, Disk herniation, Epidural
hematoma, Vertebral artery dissection,
Transverse myelitis, etc
•
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MIDDLE CEREBRAL ARTERY
• Supplies lateral surface of frontal,frontal, perital and
temporal lobes
• Most of the motor and sensory cortex Ecxept the part
on medial side and control lower limb, internal capsule
Total Occlusion:
• Uncrossed hemiplegia
• Hemianesthesia
• Global Dysphasia
• Homonymous hemianopia
• Apraxia, Agnosia
Partial occlusion:
• Any of the above features.
• Lower limb is either not or minimally involved
ANTERIOR CEREBRAL ARTERY
• Supplies MEDIAL surface of hemisphere
• Motor and sensory cortex on medial side which
control lower limb
• Soon its origin it gives a penetrating branch
(Heubner’s artery) which supply internal capsule
(containing fibers of upper limb and face)
Occlusion at the origin:
Features are similar to total occlusion of MCB
Occlusion of Heubner’s artery
:
• Weakness of upper limb and face
Occlusion after the origin of Heubner’s artery :
• Weakness of lower limb
• Loss of cortical sensory function in lower limb
POSTERIOR CEREBRAL ARTERY
• Branch of Basilar artery
• Supplies occipital lobe which include visual cortex
Occlusion:
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Visual field loss
Homonymous hemianopia
Visual agnosia
Disorders of reading
Disorders of color vision
Memory impairment
Motor dysfunction
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LATERAL MEDULLARY SYNDROME
• Also called posterior inferior cerebellar artery (PICA)
thrombosis and Wallenberg’s syndrome)
• Acommon example of brainstem infarction presenting as
acute vertigo with cerebellar and other signs. It follows
• Thromboembolism in the PICA or its branches, vertebral
artery thromboembolism or dissection.
• Features depend on the precise structures damaged.
MEDIAL MEDULLARY SYNDROME
• Characterized by a set of clinical features resulting from
occlusion of the anterior spinal artery. This results in the
infarction of medial part of the medulla oblongata.
Investigations - STROKE
The purpose of investigations in stroke is:
• To confirm the clinical diagnosis and
distinguish between hemorrhagic
and thromboembolic infarction;
• To look for underlying causes and to
direct therapy;
• To exclude other causes, e.g.
tumour.
• Sources of embolus should be
sought
Investigations of Stroke
Brain Computed Tomography (CT)
Scan
Magnetic resonance imaging (MRI)
Computed Tomography Arteriogram
and Magnetic Resonance Arteriogram:
Aneurysm, AV malformation
Carotid Ultrasound
ECG and Echocardiography
Lumber Puncture: Subarachnoid
Hemorrhage
Investigations - STROKE
 Routine bloods (for ESR, polycythaemia,
infection, vasculitis, thrombophilia, syphilitic
serology, clotting studies, autoantibodies)
 Blood Sugar Level
 Fasting Lipid profile
 Chest X-ray
 ECG and Echocardiography
 Carotid Doppler studies
 Lumber Puncture: Subarachnoid Hemorrhage
Investigations - STROKE
• Imaging in Acute Stroke.
• Non-contrast CT:
will demonstrate haemorrhage immediately but
cerebral infarction is often not detected or only
subtle changes are seen initially.
CASE SCENARIO
A 40 year old male presented in OPD
with C/O gradually progressive
weakness of both legs for the last one
month. He is also C/O backache. There
is no H/O Trauma.
There is H/O Numbness and
paresthesias in legs. He is unable to
control his urine.
CASE SCENARIO
On Examination Pulse is 84/min (regular), BP:
180/105 mm Hg.
Bulk is normal in both legs
Tone is increased in both legs,
Power is 3/5 in right leg and 2/5 in left leg.
Knee and Ankle Reflexex are Brisk bilaterally.
Both Planters are upgoing. Ankle Clonus is present
on both sides.
Upper limbs are normal.
Tenderness at back of chest.
What is your Diagnosis????
This patient has SPASTIC PARAPLEGIA
(Lesion) at T10 spinal level due to Cord
compression (aetiology). It is
complicated by bladder involvement
(functional status)
SPASTIC PARAPLEGIA
HISTORY:
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Ask about onset, duration and course of symptoms
Back pain: whether localized
Ask about radicular pain
Numbness and parasthesia particularly below the level of
lesion
Weakness: whether gradual or sudden
Sphincter control and bladder sensation
Functional status: wheelchair transfers, walking aids,
orthotic shoes and whether house has been modified for the
patient’s disability
Take a family history (hereditary spastic paraplegia)
Take a history of birth anoxia (cerebral palsy)
History of urinary infections, pressure sores and deep
venous thromboses.
SPASTIC PARAPLEGIA
EXAMINATION:
• Increased tone in both lower limbs, Hyperreflexia, Ankle
clonus
• Weakness in both lower limbs
• Then proceed to:
Check the sensory level
Examine the spine (spinal tenderness or deformity)
• Tell the examiner that you would like to do the following:
 Check sacral sensation
 Examine the hands to rule out involvement of upper
limbs
 Check for cerebellar signs (multiple sclerosis,
Friedreich’s ataxia).
SPASTIC PARAPLEGIA
EXAMINATION:
Try to localize the level of lesion using the following:
 UMNL signs in lower limb and LMNL signs in upper lims:
lesion of C5–T1.
 UMNL signs in lower limb and Wasting of small muscles of
hand: lesion of C8–T1).
 Spasticity of the lower limb alone: lesion of thoracic cord
(T2–L1).
 Flaccid Paraplegia: Lesion below L1
SPASTIC PARAPLEGIA
• Paraplegia means UMN type weakness of both lower limbs.
• CAUSES:
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Spinal Cord Compression
Transverse Mellitus
Subacute combined degenration of spinal cord
Friedreich’s Ataxia
Amyotrophic Lateral Sclerosis (MND)
Spinal cord infarction
Hereditary Spaatic parapresis
Tabes dorsalis (Neurosyphilis)
Syringomyelia
Intracranial Lesions
Parasagital Meningioma
Thrombosis of Sagittal Sinus
SPINAL CORD COMPRESSION
CAUSES
• A. EXTRADURAL:
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2.
3.
4.
5.
Vertebral Traumatic Fracture
Myeloma
Tuberculosis of Spine
Metastases (breast, prostate, lungs)
Traumatic and degenerative lesions of disc
• B. EXTRAMEDULLARY:
1. Meningioma
2. AV Malformation
• C. INTRAMEDULLARY:
Spinal Cord Tumors
SPINAL CORD COMPRESSION
Symtoms:
• H/O Backache, aggrevated by coughing, sneezing and
straining
• Pain in the distribution of nerve root
• H/O Trauma
• Weakness is usually gradually progressive except in
trauma when it is of sudden onset.
• Numbness and paresthesia in lower limbs
• Micturation-urgency or hesistancy
Signs:
• Local examination of the vertebral column may reveal
deformity or tenderness
• Sensory loss with definite upper limit
SPINAL CORD COMPRESSION
Investigations:
• X- Rays of vertebral column may show reduce disc
space, bony errosions, osteolytic or osteosclerotic
lesions, vertebral collapse or fracture.
• MRI
• Routine Investigations
TRANVERSE MYELITIS
• Inflamation of spinal cord
• Can present with paraplegia or quadriplegia
• Respiratory paralysis can occur
• Causes:
• Unknown 60 % (viral infections or postinfectious??)
• Remaining 40 % associated with autoimmune
disorders such as multiple sclerosis,
neuromyelitis optica, systemic lupus
erythematous, Sjogren’s syndrome and
sarcoidosis
TRANVERSE MYELITIS
4 classical Symptoms:
1. Backache/discomfort is first symptoms
2. Rapidly progressive weakness of lower limbs
3. Sensory symptoms such as numbness or tingling
4. Sphincter disturbances (Bladder/bowel) are common
Signs:
• UMN signs in lower limbs
• Sensory Level
Investigations:
Lumber Puncture with CSF Exam Lymphocytosis
X-Ray and MRI to rule out Cord compression
Subacute Combined Degeneration
Of Spinal Cord
• Due to Vit B12 Deficiency
• Degeneration of Posterior columns and pyramidal
tract
• Peripheral Neuropathy
Symptoms:
• Symptoms of anemia
• Gradual progressive weakness of legs
• Numbness, tingling and hyperesthesias
Signs:
• Pallor
• Paraplegia, Ankle Jerk Absent, Up going planters.
• Sense of position and vibration are lost
Subacute Combined Degeneration
Of Spinal Cord
Investigations:
• Peripheral Blood Film: Macrocytosis (MCV is raised),
Hypersegmented Neutrophils
• Pancytopenia
• Mild unconjugated hyperbilirubinemia (du to ineffective
erythropoisis.
• Serum B12 is low. Elevated LDH,
• Bonemarrow biopsy: Megaloblasts
• Schilling Test
• Causes of Vit B12 Deficiency:
• Nutritional def,, Pernicious anemia, Bacterial overgrowth
and blind loop syndrome, Diverticulosis,
Diphyllobothrium latum infestation, diseases of terminal
ileum (Crohn’s disease, ileocecal TB)
Friedreich’s Ataxia
 Familial Autosomal Recessive
 Slowly progressive degeneration of
• Posterior columns,
• Pyramidal tracts,
• Spinocerebellar tracts and
• Peripheral nerves
 Age of onset: 8 – 16 years
 Slowly progressive weakness of legs and unsteadiness
on walking
 UMN type weakness of legs
 Absent Ankle jerk
 Planters up going
 Sense of position and vibration are lost
Friedreich’s Ataxia
 Sensory Ataxia, Romberg’s sign may be +ve
 Cerebellar Signs (nystagmus, scanning speech,
intension tremors) may be present
 Associated features:
 Pes cavus (high arched foot)
 Kyphoscoliosis
 Spina Bifida
 Hypertrophic Obstructive Cardiomuopathy (HOCM)
Pes Cavus
Causes:
• Hereditary Motor and Sensory Neuropathy Type 1
(Charcot-Marie-Tooth disease)
• Friedreich's Ataxia
Causes Of Absent Ankel Jerk And Up Going
Planters:
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Friedreich's ataxia
Subacute combined degeneration of the spinal cord
Motor neurone disease
Syphilis (taboparesis)
Combined conus medullaris and cauda equina lesions
Combination of common problems e.g. diabetic
peripheral neuropathy and cervical spondylosis
CASE SCENARIO
A 65 year old male presented in OPD with
complains of slowly progressive weakness of
legs with numbness, tingling and
hyperesthesias. He is a strict vegetarian. On
examination he has spastic parapresis with
absent ankle jerk and upgoing planters.
Sense of position and vibration are lost.
His hemoglobin is 6 gm/dl.
What is most likely diagnosis?
CASE SCENARIO
Answer:
Subacute Combined Degeneration
Of Spinal Cord