1SGD07​ ​Localization​ ​in​ ​Neurological​ ​Diseases

Dr.​ ​Alreshaid
● Muscles,​ ​NMJ,​ ​nerves,​ ​plexuses,​ ​roots,​ ​and​ ​anterior​ ​horn​ ​cells​ ​of​ ​spinal​ ​cord​ ​are
all​ ​parts​ ​of>>​ ​peripheral​ ​nervous​ ​system​.
● Brain​ ​(cerebral​ ​hemisphere,​ ​cerebellum,​ ​brainstem)​ ​and​ ​spinal​ ​cord​ ​>>​​ ​CNS
● Lower​ ​motor​ ​neuron​ ​vs.​ ​upper​ ​motor​ ​neuron
Case​ ​scenario:​​ ​24​ ​y/o​ ​female,​ ​otherwise​ ​healthy,​ ​came​ ​to​ ​ER​ ​complaining​ ​of​ ​3​ ​days
history​ ​of​ ​progressive​ ​lower​ ​limb​ ​paraplegia​ ​(bilaterally)?
What​ ​is​ ​the​ ​differential​ ​diagnosis?
➢ Could​ ​be​ ​CNS:
-​ ​ ​ ​ ​Lesion​ ​below​ ​T1​ ​of​ ​spinal​ ​cord​ ​could​ ​be​ ​the​ ​cause,​ ​because​ ​the​ ​legs
are​ ​affected​ ​&​ ​everything​ ​else​ ​is​ ​not.
- Medial​ ​frontal​ ​lobe​ ​(parasagittal​ ​area)​ ​of​ ​the​ ​brain,​ ​supplied​ ​by​ ​ACA,
legs​ ​>arms
- Brain​ ​stem​ ​lesion​ ​is​ ​unlikely​ ​because​ ​there​ ​is​ ​no​ ​upper​ ​limb​ ​involvement
or​ ​cranial​ ​nerves.
-
- Not​ ​cerebellar.
➢ Could​ ​be​ ​PNS
o If​ ​muscles​ ​&​ ​NMJs​ ​are​ ​involved,​ ​it​ ​would​ ​be​ ​generalized​ ​not​ ​only
localized​ ​to​ ​legs​ ​(unlikely).
o Guillain-Barre​ ​Syndrome:​ ​may​ ​affect​ ​peripheral​ ​nerves​ ​&​ ​cause
weakness​ ​in​ ​the​ ​legs​ ​&​ ​then​ ​it​ ​ascends​ ​till​ ​it​ ​affects​ ​the​ ​arms​ ​&​ ​cranial
nerves​ ​(unlikely).
o It​ ​can​ ​be​ ​lumbo-sacral​ ​plexopathy,​ ​it​ ​is​ ​usually​ ​unilateral​ ​unless​ ​there
is​ ​a​ ​traumatic​ ​injury​ ​damaging​ ​them​ ​(unlikely;​ ​no​ ​history​ ​of
trauma).(unlikely;​ ​no​ ​history​ ​of​ ​central​ ​disc​ ​herniation​ ​of​ ​which​ ​it’d
compress​ ​cauda​ ​equine).​ ​Unilateral​ ​>​ ​bilateral
o Brucellosis​ ​(radiculopathy)​ ​may​ ​present​ ​with​ ​lumbo-sacral
involvement​ ​sparing​ ​the​ ​cervical​ ​roots
o Anterior​ ​horn​ ​cells​ ​damages:​ ​Polio​ ​>>​ ​usually​ ​affect​ ​unilateral​ ​leg​ ​and
asymmetrical​ ​(unlikely)​ ​+​ ​SMA​ ​which​ ​progresses​ ​slowly​ ​(unlikely).
● Among​ ​the​ ​above​ ​Ddx​ ​that​ ​we​ ​mentioned,​ ​the​ ​most​ ​probable​ ​cause​ ​is​ ​:
Spinal​ ​cord​ ​injury​ ​below​ ​T1​ & ​ ​ ​medial​ ​frontal​ ​lobe

Examination​ ​(start​ ​with​ ​motor):

1. Motor
● Muscles​ ​power:
● Exam:​​ ​Loss​ ​of​ ​power​ ​can​ ​happen​ ​with​ ​CNS​ ​and​ ​PNS​ ​diseases,​ ​so​ ​it’s​ ​not
helpful​ ​in​ ​differentiating​ ​between​ ​the​ ​two​ ​entities.​ ​What’s​ ​helpful​ ​is​ ​the
pattern​ ​of​ ​distribution.
POWER​ ​GRADING:

● Deep​ ​tendon​ ​reflexes​​ ​>>​ ​cause​ ​stretching​ ​the​ ​muscle​ ​spindles

● Golgi​ r​ eflexes​ ​>>​ ​stretching​ ​the​ ​tendon.​ ​(it​ ​is​ ​a​ ​protective​ ​reflux,​ ​letting​ ​go​ ​of​ ​a
heavy​ ​weight​ ​to​ ​protect​ ​the​ ​tendon​ ​from​ ​rupturing).

*N.B.​ ​Clonus​ ​happens​ ​because​ ​of​ ​the​ ​contraction​ ​of​ ​the​ ​muscles,​ ​due​ ​to​ ​the​ ​overstretch
elicited​ ​from​ ​the​ ​manual​ ​dorsiflexion​ ​of​ ​the​ ​patients’​ ​feet.
- You​ ​may​ ​have​ ​different​ ​reflexes​ ​when​ ​examining​ ​hyper​ ​reflex​ ​patients.
- Loss​ ​of​ ​power​ ​can​ ​happen​ ​with​ ​CNS​ ​and​ ​PNS​ ​diseases.
- Why​ ​does​ ​clonus​ ​happen​ ​in​ ​grade​ ​4?​ ​Normally​ ​when​ ​you​ ​stretch​ ​a​ ​muscle​ ​with
your​ ​hand,​ ​it​ ​will​ ​not​ ​elicit​ ​a​ ​reflex.​ ​But​ ​in​ ​grade​ ​4,​ ​when​ ​you​ ​have​ ​hyper
reflexia,​ ​even​ ​this​ ​small​ ​amount​ ​of​ ​electricity​ ​will​ ​be​ ​enough​ ​to​ ​stimulate​ ​the
AHC,​ ​and​ ​it​ ​keeps​ ​going​ ​on​ ​and​ ​on.

-Why​ ​do​ ​we​ ​have​ ​hyper​ ​reflexia​ ​in​ ​CNS​ ​disease?​​ ​Because​ ​the​ ​UMN​ ​goes​ ​to​ ​the
AHC​ ​and
- inhibits​ ​it,​ ​so​ ​it​ ​will​ ​remove​ ​the​ ​inhibition,
- Why​ ​do​ ​we​ ​get​ ​hyporeflexia/areflexia​ ​in​ ​LMN​ ​(PNS)​ ​disease​:​ ​If​ ​you​ ​cut​ ​the
route​ ​anywhere​ ​(muscle,​ ​plexus,​ ​nerve,​ ​root),​ ​the​ ​electrical​ ​impulse​ ​will​ ​not
conduct​ ​to​ ​and​ ​from​ ​the​ ​SC.
Tone:​​ ​is​ ​the​ ​resting​ ​basal​ ​level​ ​of​ ​muscle​ ​contractility.​ ​All​ ​muscles​ ​are
contracting​ ​all​ ​the​ ​time,​ ​even​ ​when​ ​we​ ​are​ ​relaxed,​ ​why?​ ​Because​ ​the​ ​anterior
horn​ ​cells​ ​are​ ​constantly​ ​firing​ ​(basal​ ​level).​ ​Tone​ ​is​ ​when​ ​you​ ​feel​ ​a​ ​resistance
while​ ​you​ ​apply​ ​a​ ​passive​ ​movement​ ​on​ ​a​ ​patient,​ ​because​ ​there​ ​is​ ​a​ ​basal
level​ ​of​ ​contractility.​​ ​It​ ​can​ ​differentiate​ ​PNS​ ​vs​ ​CNS.
o CNS​ ​disease,​ ​you​ ​will​ ​remove​ ​the​ ​inhibition​ ​of​ ​UMN>>>>​ ​hyper​ ​tonicity.
o Spastic​ ​hypertonicity:​​ ​increased​ ​tone​ ​due​ ​to​ ​pyramidal
/corticospinal​ ​dysfunction.​ ​Clinically​ ​there​ ​is​ ​resistance​ ​in​ ​the
beginning​ ​then​ ​it​ ​gives​ ​away​ ​when​ ​pulling​ ​(Clasp-knife
phenomena)
o Rigid​ ​hypertonicity:​​ ​increase​ ​tone,​ ​due​ ​to​ ​extrapyramidal​ ​(e.g.
basal​ ​ganglia)​ ​damaged.​ ​Clinically,​ ​the​ ​tone​ ​is​ ​increased
throughout​ ​the​ ​whole​ ​movement​ ​(lead-pipe​ ​phenomena).
Resistance​ ​is​ ​uniform​ ​throughout​ ​the​ ​movement.​ ​Cogwheel
tremors​ ​are​ ​seen​ ​in​ ​Parkinson​ ​→​ ​rigidity​ ​+​ ​tremors.
o PNS​ ​disease​ ​>>>>decrease/​ ​no​ ​tone​ ​(flaccid)
o Examine​ ​tone​ ​by​ ​asking​ ​the​ ​patient​ ​to​ ​relax​ ​and​ ​attempt​ ​moving​ ​the​ ​joint
quickly.
● Check​ ​Babinski​ ​sign/​ ​Plantar​ ​reflex​:​ ​if​ ​positive​ ​(toes​ ​go​ ​up​ ​or​ ​fanning​ ​)​ ​means
CNS​ ​disease​ ​not​ ​PNS​ ​(will​ ​go​ ​down​ ​/negative)​ ​–​ ​Hoffman’s​ ​for​ ​the​ ​hand.

2. Sensory​​ ​loss​ c​ an’t​ ​help​ ​you​ ​in​ ​distinguishing​ ​peripheral​ ​vs​ ​central​ ​disease
because​ ​it​ ​happens​ ​in​ ​both​ ​&​ ​it​ ​is​ ​totally​ ​subjective,​ ​but​ ​the​ ​DISTRIBUTION​ ​of
sensory​ ​loss​ ​can​ ​help​ ​in​ ​localization​ ​*Came​ ​as​ ​an​ ​exam​ ​question​ ​for​ ​the​ ​boys.
Pointers:
● How​ ​can​ ​you​ ​differentiate​ ​between​ ​brain​ ​&​ ​spinal​ ​cord​ ​disease​ ​(in​ ​general)?
o If​ ​brain:​ ​other​ ​problems​ ​like​ ​speech​ ​problems,​ ​swallowing,​ ​and​ ​facial
weakness,​ ​cognitive​ ​function,​ ​mental​ ​status.
o If​ ​in​ ​spinal​ ​cord:​ ​everything​ ​else​ ​above​ ​cervical​ ​spine​ ​(neck)​ ​is​ ​normal.
Exception:​ ​Horner’s​ ​disease.
● Brainstem​ ​vs​ ​Cerebral​ ​lesions:
➢ Brain​ ​stem​ ​lesion:
▪ More​ ​Cranial​ ​nerves​ ​symptoms.
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▪ Bilateral​ ​symptoms
▪ Crossed​ ​deficit​:​ ​means​ ​having​ ​Cranial​ ​nerves​ ​symptoms​ ​in​ ​one​ ​side
with​ ​contralateral​ ​weakness.​ ​For​ ​example,​ ​someone​ ​having​ ​pontine
lesion​ ​damaging​ ​facial​ ​nucleus​ ​on​ ​right​ ​side​ ​of​ ​pons:​ ​he’ll​ ​have​ ​right
side​ ​facial​ ​weakness​ ​&​ ​contralateral​ ​hemiplegia​ ​(because​ ​the​ ​fibers
decussate​ ​in​ ​the​ ​lower​ ​medulla,​ ​if​ ​it​ ​was​ ​above​ ​the​ ​pons​ ​it​ ​will​ ​be
ipsilateral).​*​Exam​ ​question
➢ Cerebral​ ​hemisphere​ ​lesion:
▪ Cognitive​ ​dysfunction.
▪ Usually​ ​unilateral.
● Cortical​ ​vs​ ​Subcortical​ ​lesions:
➢ Hemiplegia​ ​+​ ​normal​ ​language​ ​(understand​ ​&​ ​can​ ​talk)​ ​=​ ​subcortical​ ​lesion
➢ Hemiplegia​ ​+​ ​aphasia​ ​(can’t​ ​understand​ ​or​ ​can’t​ ​talk)​ ​=​ ​cortical​ ​lesion
➢ Cortical​ ​sensory​ ​modalities,​ ​Primitive​ ​(light​ ​touch,​ ​temp,​ ​vibration)​ ​&​ ​others
(like:​ ​graphesthesia,​ ​stereognosia,​ ​2​ ​point​ ​discrimination​)​ ​>>all​ ​are​ ​cortical
functions​.​*Exam​ ​question
▪ Stereognosia:​ ​acknowledging​ ​things​ ​by​ ​touching​ ​them​ ​(3D
knowledge)
▪ Graphesthesia:​ ​writing​ ​a​ ​number​ ​on​ ​your​ ​hand​ ​with​ ​closed​ ​eyes>​ ​you
will​ ​feel​ ​it​ ​in​ ​both:
● if​ ​you​ ​knew​ ​which​ ​letter​ ​it​ ​is>>​ ​this​ ​means​ ​you​ ​have​ ​an​ ​intact
cortex
● if​ ​you​ ​didn’t​ ​understand​ ​which​ ​letter​ ​it​ ​is>>​ ​cortex​ ​lesion
(agraphesthesia)
Note:​​ ​There​ ​is​ ​a​ ​difference​ ​between​ ​speech​ ​and​ ​language.
Language​ ​is​ ​a​ ​higher​ ​cortical​ ​function​ ​(phonation)​ ​whereas​ ​speech​ ​(articulation)​ ​is
primitive​ ​hence​ ​subcortical.