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Localizing Neurological Lesions

1. The document outlines key questions and signs for neurological problems including determining if there is a neurologic deficit, localizing the lesion, determining the nature of the lesion, and deciding on treatment. 2. It discusses signs of increased intracranial pressure like headache, diplopia, vomiting, and papilledema. Meningeal irritation signs include nuchal rigidity, Kernig's sign, and Brudzinski's sign. 3. Lesion localization depends on whether deficits are contralateral for supratentorial or ipsilateral for infratentorial lesions. Spinal cord lesions can be localized by dermatomal sensory deficits and lower extremity weakness or bowel/bladder problems.

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Pramod Thapa
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0% found this document useful (0 votes)
316 views6 pages

Localizing Neurological Lesions

1. The document outlines key questions and signs for neurological problems including determining if there is a neurologic deficit, localizing the lesion, determining the nature of the lesion, and deciding on treatment. 2. It discusses signs of increased intracranial pressure like headache, diplopia, vomiting, and papilledema. Meningeal irritation signs include nuchal rigidity, Kernig's sign, and Brudzinski's sign. 3. Lesion localization depends on whether deficits are contralateral for supratentorial or ipsilateral for infratentorial lesions. Spinal cord lesions can be localized by dermatomal sensory deficits and lower extremity weakness or bowel/bladder problems.

Uploaded by

Pramod Thapa
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
  • Neurological Examination and Deficit Localization

NEUROLOGY II KC GANDA

DR. FRANZ RASAY


4 Questions for Neurological Problem:

1.) Is there a neurologic deficit? 3 signs of meningeal irritation:


2.) Where is the lesion? --> Levelize, Lateralize,
Localize  Nuchal rigidity: resistance of passive flexion of
3.) What is the nature of the lesion? the neck forward.
4.) What can we do? o When there is resistance laterally, and
resistance on forward flexion = cervical
 IS THERE A NEUROLOGIC DEFICIT? paratonia (secondary to prolonged
A. Presence of focal deficit bedridden patient)
 Kernig’s sign: “Knee”
 Dependent on what part of NS is affected
o (+) electric shock or pain in the back area or
 Involves the cerebral or supratentorial =
cervical area
memory deficit, seizure (cortical area),
 Brudzinski Sign: :Batok”
headache
o Passive flexion of the neck
 HAVE A COMPLETE HISTORY AND P.E & neuro
o *****
exam
 Presence of problem in the supratentorial DIFFERENTIATE:
area like Headache, Seizure, Memory
problem, Behavioral changes/ mood o Meningitis: (+) Fever
symptoms o Subarachnoid hemorrhage: thunderclap
 Presence of cranial deficit HA/ worst HA of patient’s life
[INFRATENTORIAL] = sudden visual loss
particularly unilateral ; Diplopia= EOM  Dizziness: disorientation of one’s self to space,
(3,4,6) involved; Sensory deficit= CN 5; time, place
Facial asymmetry= CN 7; Impairment of
Peripheral Dizziness Central Dizziness
muscle of mastication = CN 5; Ptosis = CN
Rotatory Non- rotatory
3; Bell’s palsy = CN 7 (closing of eyes); Feeling of unsteadiness/
Dysphagia = CN 9/10; Dysarthria = CN 12 imbalance
 Weakness: impairment or decrease in Hearing deficit, tinnitus (-)
motor strenghth (Upper or lower extremity Horizontal nystagmus Vertical nystagmus &
weakness; Bilateral lower extremity Horizontal nystagmus
weakness= quadriplegia ) (+) cereberal signs:
dysmetria,
 Sensory deficit: Numbness, tingling
 ALL INFRATENTORIAL LESION = IPSILATERALLY
sensation
 ALL SUPRATENTORIAL LESION =
B. Presence of signs & symptoms
CONTRALATERALLY
 Increase ICP:
a. headache
 Where is the lesion?
b. Diplopia secondary to lateral rectus
 Levelize: Supra/ Infra (cranial deficit, cerebellar
palsy (deviation to the right)
deficit, spinal cord)
c. Vomiting
 Lateralize: Right / Left
d. Papilledema
 Localize: what part of NS is affected
C. Presence of meningeal irritation
 CNS Infection: Meningitis
Patient with right facial asymmetry & RS weakness:
 Subarachnoid Hemorrhage: flooded
Levelize?
with flood in the subarachnoid area
o Motor & sensory system deficit : contralateral WEAKNESS
o Both upper & lower part of the face: peripheral UPPER MOTOR NEURON LOWER MOTOR NEURON
palsy: Infratentorial Spasticity Flaccid
o Central facial palsy: deficit is in Supratentorial Hyperreflexive Hyporeflexive
area affecting the lower part of the face (+) Babinski (-) Babinski
Clonus (-)
because of double innervation
(-) Fasciculations
o Facial palsy on the left & weakness on the right:
o Delineation of UMN/ LMN?
cross deficit = Infratentorial area
o UPM: Motor cortex
o LMN: Anterior Horn Cell, Peripheral nerves,
 RS WEAKNESS, eyes mediated laterally= Medial
Neuromuscular junction, Muscle
rectus is affected CN3, Brainstem
Infratentorial
AHC PN NMJ M
Pure motor Mixed type Motor Mixed
FRONTAL LOBE SIGNS: (weakness) Distal motor Segmental Fluctuating Proximal
1. Grasp reflex problem sensory Problem
2. Palmomental reflex problem
3. Pout reflex (+) PAIN
4. Rooting reflex (+) (+)
5. Glabellar signs Fasciculation Fasciculation
**
dependent
PARIETAL LOBE SIGNS: on the
1. Right to Left Disorientation nerve
2. Agraphia affected
3. Finger agnosia
4. Agraphesthesia
 58 Y/O M, HTNsive, RS weakness, Lateral rectus
TEMPORAL LOBE SIGNS: palsy on the left, hyperreflexive:
o Silent areas - Levelize? INFRA
o SEIZURES- hyperactive neurons - Lateralize? LEFT
- Localize: Metencephalon
OCCIPITAL LOBE SIGNS:  On neuro exam, the ptn presents with HA, on
o Visual problems cortical mapping, you put a coin on the left
hand of the patient & did not identify the object
SPINAL CORD LESION: - What deficit? Astereognosis
1. Bilateral lower extremity weakness  Lateralize the lesion: Right (contralateral)
(Quadriplegia):  Ptn due to bilateral lower extremity weakness,
-ex: thoracic & lumber: quadriplegia neuro exam 0/5 on both extremities, 5/5 on
Cervical area: arms & legs upper, deficit in T10 area of pain & temperature
2. Definite sensory loss: dermatomal mapping is deficit, proprioception & vibration & fine
(T10) but move 2 spinal cord level up touch is intact, Babinski on bilateral lower ext
3. Urinary/ Bowel problem: S2-S4 lesion (anal (+), hyperreflexia
sphincter) - Lateralize: Either R & L
- Localize: T8

KC GANDA
NEUROLOGY II KC GANDA
DR. FRANZ RASAY
SPINAL CORD

 Posterior Funinculus: Cuneate tract & Gracilis


tract= innervate proprioception & vibration  Secondary to LE weakness, hyporeflexia, (-)
 Lateral funiculus: Lateral spinothalamic tract = Babinski,flaccidity, (-) fasciculation,
pain & temperature segmental sensory problem
 Anterior funiculus: Anterior spinothalamic tract = - NEITHER because spinal cord
fine/ light touch - EMG-NCD: Electromyogram Nerve
conduction = for lower motor neuron deficit
 23 y/o UE weakness, inability to comb hair, neuro HEADACHE
exam: hyporeflexia, flaccidity on R ue, atrophy, (-) - Any pain/ discomfort in between the glabella/
Babinski occipital protuberance
- Localize: Muscle
 Noted fasciculations, distal weakness  Different pain sensitive structures:
- LOCALIZE: Muscle - Extracranial: outside the skull: skin, sinuses,
- Exception: distal myopathy eye, subq area, nasal area, ears, nasal
cavity
- Intracranial: inside the skull:
III. What is the nature of the lesion?
 Vessels
 Vascular: Stroke (sudden)
 Cavernous sinus or other sinuses
 Infection
 Dura & other meninges
 Toxic: ex. Pb poisoning, APAP
 Spinal nerves: cervical nerves
 Autoimmune: dermatomyositis, stroke
secondary to SLE
 Metabolic: ptn w/ multiple vomiting:
Hypokalemia
 Inflammatory: GBS/ AIDE  1st thing to do is to delineate if it is:
 Neoplastic: Vascular is sudden, Neoplastic is - Secondary HA: structural problems inside
progressive the brain; ex. Tumor, blood
 Congenital: hydrocephalus  Systemic illness: patient with HIV/ Ca
 Degenerative: Alzheimer’s disease  Neurologic problem
 Onset: ex. sudden severe HA=
*Plain CT Scan: Stroke- Bleed (with HA, high BP) subarachnoid
*Plain MRI: Infarct  Old patient: tumor
 Progressive: have a large tumor
 RS weakness, sudden onset  YES: 1 or more symptoms = secondary
-Stroke type
-Plain MRI
- Primary HA: not secondary to structural
 Progressive HA & weakness, secondary signs inside the brain
sensorium, vomiting, severe HA 1.) MIGRAINE
-Neoplastic 2.) Tension HA
-MRI w/ contrast 3.) Cluster HA

KC GANDA
EPIDEMIOLOGY CLINICAL PATHOLOGY DIAGNOSIS TREATMENT OTHERS
MANIFESTATION

1.) MIGRAINE

Common At least 2 out of 4:


Migraine - Young “PUMA”  Familial: very sensitive artery  No  Abortive treatment:
adults  Pulsating causing pulsation of external diagnostic -NSAIDS
- W>M  Unilateral carotid artery = dec. cerebral tool
 Moderate in blood flow = cortical  Prophylactic treatment:
severity spreading depression (prevent the
 Activity in daily  This release chemicals like: occurrence, 2 or more
living CGRP, Peptides, Substance B, HA per week that
impairment Glutamate impair activities of
 Activating trigeminal vascular living)
system - Anti- convulsant:
 Activation is secondary to Valproic Acid, CBZ
some precipitant: coffee, - Anti- depressants:
fatigue/ lack of sleep Amytriptillin
- Beta blocker: -olols
- ARBS: -sartans
Neurogenic  Aura
Migraine

Complicated  Pulsating,  Prophylactic treatment  Stroke


Migraine unilateral mimickers:
 Numbness BUT all
 Slurring of speech neurologic
abnormalities
subsides
 Can lead to
migranous
infarct because
of prolonged
constriction of
blood vessel
KC GANDA
NEUROLOGY II KC GANDA
DR. FRANZ RASAY
can cause
stroke

Status - Lasts 72 hrs - IV Steroids


Migranosus - 3-4 days/ - Other Anti
week, convulsant
continuous - Hydrate patient
2.) TENSION  Young adult Opposite of PUMA  Secondary to contraction of - CLinical - Anti-depressant - Associated
HA & early  Non pulsating different muscles  (Amytriptyline) with anxiety,
adulthood  Bilateral impinge different nerves depression &
 W =M  Mild to moderate (cervical/ trigeminal)  fatigue
in severity HEADACHE
 Will not impair
activity in daily
living
3.) Cluster HA  Young  Periorbital area  Unknown -CLinical  Diagnostic &
aka. Alarm Adult associated with  Associated with CN 5 Therapeutic: 100%
clock HA  Men lacrimation OXYGEN
 -TRIPTANS
MISCELLANEOUS HA

1.) Trigeminal - MRI W/ - Carbamazepine  Painful event


Neuralgia - Stab like, electric - Idiopathic MRA >MOA: Na blocker in neuro
- Aka: Tic shock like pain - Non idiopathic: Vascular roots  Affects the V2
Douloureux over the facial of Basilar Artery (Mandibular)
area & V3
(Maxillary)
 Associated with
Multiple
sclerosis, CT
Angle tumor &
Aneurysm of
Basilar Artery

KC GANDA
2.) Herpes - Secondary - Eye: Herpes Zoster - Antiviral -
Zoster to a virus Ophthalmicus - Anti depressant
- Aka: post - Ear: Herpes Zoster Auricularis - Anti convulsant
herpectic - Ramsay Hunt Syndrome:
neuralgia Vesicles in the pinna/
external auditory canal w/
associated deafness &
dizziness
3.) Trochlear - CN 4 -Superior oblique muscle with - Carbamazepine
Neuralgia innervates intort eye medially 
SO ADDUCTION = pain in
superomedial area
4.) Vago- - Pain upon - Carbamazepine
glossophary swallowing
ngeal
neuralgia
5.) Costen - Secondary - Most common cause: - Amitriptyline
Syndrome to pain on malocclusion of dentures - Anti convulsant
chewing or - Secondary to irritation of
trigeminal nerve
6.) Temporal - > 60 y/o - Can ;ead to - HA in temporal area - ESR ( > - Steroids
Arteritis - Male blindness - Can cause occlusion of 50mm/
headache in ophthalmic artery hr)
temporal
area
prominent,
tender,
pulsating

KC GANDA

NEUROLOGY II 
 
KC GANDA 
DR. FRANZ RASAY 
4 Questions for Neurological Problem: 
1.) Is there a neurologic deficit? 
2.) Whe
KC GANDA 
 
 
o Motor & sensory system deficit : contralateral 
o Both upper & lower part  of the face: peripheral 
palsy: In
NEUROLOGY II 
 
KC GANDA 
DR. FRANZ RASAY 
KC GANDA 
 
SPINAL CORD 
 
Posterior Funinculus: Cuneate tract & Gracilis 
tract=
KC GANDA 
 
EPIDEMIOLOGY 
CLINICAL 
MANIFESTATION 
PATHOLOGY 
DIAGNOSIS 
TREATMENT 
OTHERS 
1.) MIGRAINE 
 
 
 
Common 
Migra
NEUROLOGY II 
 
KC GANDA 
DR. FRANZ RASAY 
KC GANDA 
 
can cause 
stroke 
Status 
Migranosus 
- Lasts 72 hrs 
- 3-4 days/ 
we
KC GANDA 
 
2.) Herpes 
Zoster 
- 
Secondary 
to a virus 
- 
Aka: post 
herpectic 
neuralgia 
 
- Eye: Herpes Zoster 
Ophthal

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