Here are the key points to differentiate upper motor neuron (UMN) and lower motor neuron (LMN) facial nerve lesions:UMN lesion:- Milder weakness as some fibers are spared- Forehead is spared as it is innervated by upper branches directly from CN VII nucleus - Bell's phenomenon (automatic closure of eye on attempted smile) is preservedLMN lesion:- Complete paralysis of muscles of expression on affected side- Forehead is involved as it receives branches from main facial trunk- Bell's phenomenon is absent as motor fibers to the orbicularis oculi are disruptedSo in summary:- UMN lesion spares forehead and preserves Bell's phenomenon
The document discusses the central nervous system and cranial nerves. It provides details on the structure and function of the brain, spinal cord, and cranial nerves I-VII. It describes signs and symptoms of damage to different parts of the central nervous system as well as clinical tests to evaluate cranial nerves and localized lesions. Bitemporal hemianopsia is listed as the visual field defect that would result from a pituitary tumor expanding superiorly.
Similaire à Here are the key points to differentiate upper motor neuron (UMN) and lower motor neuron (LMN) facial nerve lesions:UMN lesion:- Milder weakness as some fibers are spared- Forehead is spared as it is innervated by upper branches directly from CN VII nucleus - Bell's phenomenon (automatic closure of eye on attempted smile) is preservedLMN lesion:- Complete paralysis of muscles of expression on affected side- Forehead is involved as it receives branches from main facial trunk- Bell's phenomenon is absent as motor fibers to the orbicularis oculi are disruptedSo in summary:- UMN lesion spares forehead and preserves Bell's phenomenon
Similaire à Here are the key points to differentiate upper motor neuron (UMN) and lower motor neuron (LMN) facial nerve lesions:UMN lesion:- Milder weakness as some fibers are spared- Forehead is spared as it is innervated by upper branches directly from CN VII nucleus - Bell's phenomenon (automatic closure of eye on attempted smile) is preservedLMN lesion:- Complete paralysis of muscles of expression on affected side- Forehead is involved as it receives branches from main facial trunk- Bell's phenomenon is absent as motor fibers to the orbicularis oculi are disruptedSo in summary:- UMN lesion spares forehead and preserves Bell's phenomenon (20)
High Profile Call Girls Coimbatore Saanvi☎️ 8250192130 Independent Escort Se...
Here are the key points to differentiate upper motor neuron (UMN) and lower motor neuron (LMN) facial nerve lesions:UMN lesion:- Milder weakness as some fibers are spared- Forehead is spared as it is innervated by upper branches directly from CN VII nucleus - Bell's phenomenon (automatic closure of eye on attempted smile) is preservedLMN lesion:- Complete paralysis of muscles of expression on affected side- Forehead is involved as it receives branches from main facial trunk- Bell's phenomenon is absent as motor fibers to the orbicularis oculi are disruptedSo in summary:- UMN lesion spares forehead and preserves Bell's phenomenon
2. Central nervous system (CNS)– includes the
brain and spinal cord
Peripheral nervous system (PNS)–
composed of the muscles ,NMJ , peripheral
nerves (( cranial and spinal nerves)), roots
and plexuses
Autonomic system – comprises the
sympathetic and parasympathetic system
(controls smooth muscle action)
3.
4. Forebrain – cerebrum and diencephalon
Midbrain – mesencephalon
Hindbrain – cerebellum,pons and the
medulla oblongata (sometimes called the
brain stem)
5. Signs of UMN Upper Motor Neuron damage:
1- Muscle weakness.
2- Hypertonia ----------spasticity.
3- Hyperreflexia.( deep tendon reflex) +/- clonus.
4- Babinski sign
5- Absent abdominal & cremasteric reflexes
6- In long standing cases there is wasting( disuse).
7- Spasticity is hallmark of the UMN disease.
Spasticity is a state of sustained increase in muscle
tension in response to muscle lengthening, in
particular, with passive movements.
8-Pseudobulbar palsy is hallmark of the UMN
disorder
6. Signs of LMN lesions
1.Weakness or paralysis of muscles
2- Hypotonia
3- Absent tendon reflexes (Hyporeflexia).
4- Fasciculation
5- Absent or flexor planter response
6- Muscle wasting.
7. Localization of level of UMNL
Sites = Brain , Brain stem , Spinal cord
1- Cortical lesions localized loss of
function e.g. monoplegia, aphasia,
apraxia
2- Internal capsule ---- hemiplegia
3- Brain stem lesions ----- crossed
hemiplegia
4- Spinal cord lesions ------ Ipsi-lateral
weakness.
8. ((ANTERIOR CIRCULATION))
Higher Cortical Function
Aphasia, Apraxia , Agnosia
Cranial Nerves: normal except 7th
&unless
forced eye deviation
cerebellar Function: normal
Motor:
Weakness of face/arm>leg (or vice versa)
Sensory:
Sensory abnormality of face/arm>leg
Deep Tendon Reflexes:
Hyper-reflexia Babinski’s reflex
9.
10. ((POSTERIOR CIRCULATION))
Higher Cortical Function: normal
Cranial Nerves:
III, IV, VI: Diplopia
V: Decreased facial sensation
VII: Drooping of nasolabial fold.
VIII: Deaf and Dizzy
IX, X, XII: Dysarthria and Dysphagia
XI: Decreased strength in neck and shoulders
Cerebellar Function: usually normal
Motor: hemi-paresis ( crossed)
Sensory: hemi-dysesthesias ( crossed).
Deep Tendon Reflexes: hemi-hyper-reflexia.
Pathologic Reflexes: Babinski’s reflex
11. CEREBELLUM
Higher Cortical Function: normal
Cranial Nerves: usually normal
Cerebellar Function:
Nystagmus
Flaccid dysarthria
Motor:
Normal bulk and strength with ipsilateral hemi-hypotonia
Intention tremor
Axial instability with dysmetria
Sensory: Normal
Deep Tendon Reflexes: Normal
Pathologic Reflexes: Normal
(plantar flexing to plantar stimulation
12. ((SPINAL CORD LESION))
Higher Cortical Function: normal
Cranial Nerves: normal
Cerebellar Function: normal
Motor:
weakness (extensors worse than flexors) below the lesion
Hypertonia below the lesion with spasticity
Sensory:
horizontal level usually lower than the lesion, poorly
localizing , may be somewhat asymmetric
Deep Tendon Reflexes:
Hyper-reflexia below the level, possibly clonus
Pathologic Reflexes:
loss of superficial reflexes (abdominal, cremasteric, anal
wink)
Babinski’s reflex
17. Test with alcowipes, coffee .
Unilateral anosmia may be significant
Bilateral anosmia: commonest cause viral
Classical pathology:olfactory groove
meningioma
Basal skull fractures another potential cause
(unilateral or bilateral)
18. Optic Nerve II
Provides vision
Damage causes blindness in visual field
20. VISUAL ACUITY
CORRECTED (ie brain not lens)
Each eye separately
Snellen charts for distance and near vision
reading charts for near vision
If unable, finger counting, hand movements,
perception of light
21. VISUAL FIELDS
Often forgotten but very important
First do a bilateral screening test: will uncover
the majority of significant visual field defects
immediately
Go on to check each eye separately, ask
about scotomata
Mention checking for blind spot enlargement
22.
23.
24. COMMON FIELD DEFECTS
HOMONOMOUS HEMIANOPIA: lesion
posterior to the optic chiasm (eg posterior
cerebral artery territory infarction)
BITEMPORAL HEMIANOPIA: lesion at the
optic chiasm (eg pituitary tumour)
BLINDNESS ONE EYE: lesion in eye, retina
or optic nerve
25. PUPILLARY RESPONSES
Light reflex is the clinically significant one
Afferent limb = II, efferent limb = III
Look at pupillary sizes
Direct and consensual response
Look for afferent pupillary defect (optic nerve
lesion)
26. One large pupil: IIIrd nerve palsy, iris problem
(eg traumatic midriasis), unilateral dilator eye
drops
Small pupil: Horner’s syndrome, Argyll-
Roberston pupil (small, irregular, reacts to
accommodation but not to light)
Bilateral small pupils: drugs (opiates), pontine
lesion (haemorrhage
27. HORNER’S SYNDROME
Oculosympathetic paralysis
A good lateralising sign but a poor localising
sign
Ptosis, miosis and sometimes unilateral
anhydrosis of face
Look especially at neck, supraclavicular
fossa and hand (Pancoast’s tumour)
28. . A patient who has been exhibiting various
endocrine abnormalities has an MRI scan of the
head. This scan reveals a small tumor of the
pituitary gland. As this tumor expands superiorly
what visual field defect will this patient exhibit?
A. Left or right monocular blindness
B. Binasal hemianopsia
C. Left or right homonymous hemianopsia
D. Bitemporal hemianopsia
29.
30.
31. Eye movements (III, IV and VI)
III: OCULOMOTOR NERVE: all
extraocular muscles,Except SO & LR ,
Also carries parasympathetic (constrictor)
fibres to pupil, and
Fibres to levator palpebrae superioris
32. Look at eyes in primary position of gaze
IIIrd nerve palsy: ptosis ,eye often ‘down and out’
VI nerve palsy: often eyes convergent
(unopposed medial rectus)
Look at pupils
Look for ptosis
33. Oculomotor Nerve III
Somatic and Autonomic motor function
Eye movement (Superior, inferior, medial rectus muscles and inferior
oblique muscle), opening of eyelid (levator palpebrae superioris),
constriction of pupil (circular muscle), focusing (ciliary muscle and
accomodation)
34. Fibers extend from the ventral midbrain, pass
through the superior orbital fissure, and go to the
extrinsic eye muscles
Functions in raising the eyelid, directing the
eyeball, constricting the iris, and controlling lens
shape
The latter 2 functions are parasympathetically
controlled
Parasympathetic cell bodies are in the ciliary
ganglia
35. Damage causes
1. Drooping eyelid ((ptosis))
2. Dilated pupil
3. Double vision
4. Difficulty focusing and inability to move
eye in certain directions
5. Down and out {{eye}}
36.
37. Trochlear Nerve IV
Eye movement (superior oblique muscle)
Damage causes double vision and inability to
rotate eye inferolaterally
38. Abducens Nerve VI
Provides eye movement (lateral rectus m.)
Damage results in inability to rotate eye
laterally and at rest eye rotates medially
39.
40.
41. Diagnosing complete 6th cranial nerve palsies is easy,
but determining their etiology can be more challenging.
Excluding increased intracranial pressure and
papilledema (by looking for retinal venous pulsations
during funduscopy) is important. MRI or CT can help
exclude intracranial mass lesions, hydrocephalus, and
direct nerve compression by lesions in the orbit,
cavernous sinus, and base of the skull. Lumbar puncture
determines the CSF opening pressure and can detect
leptomeningeal inflammatory, infectious, or neoplastic
infiltrates entrapping the 6th nerve. A collagen vascular
screen helps exclude a vasculopathic process. In many
cases, 6th nerve palsies resolve once the primary
disorder is treated.
44. Most important function is sensory
Ophthalmic, maxillary and mandibular divisions
Test with light touch and pinprick in all 3
divisions, comparing each side
Corneal reflexes (afferent limb V, efferent limb
VII)
Know something about trigeminal neuralgia
(examination is normal in these cases)
45. Ophthalmic branch – sensations from nasal
cavity, skin of forehead, upper eyelid, eyebrow,
nose
Maxillary branch – sensations from lower eyelid,
upper lips and gums, teeth of the maxilla, cheek,
nose, palate, pharynx
Mandibular branch – sensations from teeth of
the mandible, lower gums and lips, palate,
tongue. Motor function of temporalis and
masseter muscles.
Damage produces loss of sensation and
impaired chewing
46. Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)
Fibers run from the face to the pons via the
superior orbital fissure (V1), the foramen
rotundum (V2), and the foramen ovale (V3)
Conveys sensory impulses from various areas of
the face (V1) and (V2), and supplies motor fibers
(V3) for mastication
Tic douloureux or trigeminal neuralgia
- Most excruciating pain known (?)
- Caused by inflammation of nerve
50. Motor - facial expressions
Autonomic Motor - salivary and lacrimal
glands, mucous membranes of nasal and
palatine mucosa
Sensory - taste on anterior 2/3’s of tongue
Damage produces sagging facial muscles
and disturbed sense of taste (no sweet
and salty)
51. DIFFERENTIATE AN UPPER MOTOR
NEURON FROM A LOWER MOTOR
NEURON LESION
Upper motor neuron lesion: milder, spares
the forehead, no Bell’s phenomenon
52. Branches of Facial Nerve
Clinical test: Test anterior 2/3’s of tongue with
substances such as sugar, salt,; test response of tear
glands to ammonia fumes; test motor functions by
asking subject to close eyes, smile, whistle, frown, raise
eyebrows, etc.
53. Upper facial territory is supplied by bilateral motor
cortices
Lower facial territory is supplied only by contralateral
motor cortex
Therefore, unilateral central lesions spare upper face
Lesions distal to geniculate ganglion
Mostly motor abnormalities
Lesions proximal to geniculate ganglion
Motor, gustatory & autonomic abnormalities
54.
55. Bell's Palsy
Unilateral facial paralysis of sudden onset
Unknown cause.
The mechanism presumably involves
swelling of the nerve due to immune or
viral disease, with ischemia and
compression of the facial nerve in the
narrow confines of its course through the
temporal bone.
56. Symptoms of Bell’s Palsy
--Symptoms usually start suddenly, and range from mild to severe. They may
include:
Twitching in face
Weakness in face
Face feels stiff or pulled to one side
Droopy eyelid or corner of mouth
Drooling due to inability to control facial muscles
Facial Paralysis of one side of the face, makes it hard to close one eye
Change in facial expression (for example, grimacing)
Dry eye or mouth
Loss of sense of taste
Difficulty with eating and drinking
Pain behind or in front of the ear, may occur 1-2 days before muscle
weakness
Sensitivity to sound (hyperacusis) on the side of the face affected
Headache
--These symptoms of Bell's palsy usually begin suddenly and reach their peak
within 48 hours
57.
58. The affected side becomes flat and
expressionless, but patients may complain
instead about the seemingly twisted intact side.
In severe cases, the palpebral fissure widens,
and the eye does not close.
The patient may complain of a numb or heavy
feeling in the face, but no sensory loss is
demonstrable. A proximal lesion may affect
salivation, taste, and lacrimation and may cause
hyperacusis.
59. Weakness of the entire half of the face
distinguishes Bell's palsy from supranuclear
lesions (eg, stroke, cerebral tumor), in which the
weakness is partial, affecting the frontalis and
orbicularis oculi less than the muscles in the
lower part of the face. Bell's palsy must be
differentiated from unilateral facial weakness
due to other disorders of the facial nerve or its
nucleus, chiefly geniculate herpes (Ramsay
Hunt's syndrome), middle ear or mastoid
infections, sarcoidosis, Lyme disease, petrous
bone fractures, carcinomatous or leukemic
nerve invasion, chronic meningeal infections,
and cerebellopontine angle or glomus jugulare
tumors
60. A 24 y. o. woman presents to her physician with an
inability to close her right eye. Physical exam reveals
weakness of the right orbicularis oculi. Which of the
following symptoms would likely also be present?
A. Double vision
B. Inability to feel the face
C. Inability to chew
D. Hyperacusis
E. Inability to shrug the shoulder
61. 61
A 49 year old woman is in a motor vehicle accident and sustains a
closed head injury. A CT scan does not show any intracranial
hemorrhage but reveals a small tumor at the cerebellopontine angle
of the brain. Which of the following nerves is most likely to be
affected by this tumor?
A. Facial nerve
B. Glossopharyngeal nerve
C. Abducens nerve
D. Trigeminal nerve
E. Vagus nerve
62. Vestibulocochlear Nerve VIII
Special Sensory
Provides hearing (cochlear branch) and sense of
balance (vestibular branch)
Damage produces deafness, dizziness, nausea,
loss of balance and nystagmus
63. For clinical examination purposes, forget the
vestibular element
Check hearing approximately in each ear
If reduced, determine whether conductive
(BC >AC) or sensorineural (AC>BC)
deafness
64.
65. GLOSSOPHARYNGEAL (IX) AND
VAGUS (X)
Tested together
Speech, palate, cough, swallow, (gag reflex)
Bulbar palsy: bilateral LMN lesions of IX and
X: poor palatal movement, nasal speech,
nasal regurgitation of fluids
Pseudobulbar palsy: bilateral UMN lesions:
‘hot potato’ speech, no nasal regurgitation,
additional frontal lobe signs
66. Glossopharyngeal Nerve IX
Somatic motor – Swallowing and voice production via pharyngeal
muscles
Autonomic motor - salivation, gagging, control of BP and respiration
Sensations from posterior 1/3 of tongue including taste
Sensations from baroreceptors and chemoreceptors
Damage results in loss of bitter and sour taste and impaired swallowing,
blood pressure anomalies (with CN X).
67.
68. 68
A physician is performing a cranial nerve exam on a patient.
While testing the gag reflex it is noted that when the left side of the
pharyngeal mucosa is touched, the patient gags and his uvula
deviates to the left. When the right side is touched, the patient
does not gag. Which of the following is the most likely location of
his lesion?
A. Left glossopharyngeal and vagus nerves
B. Right glossopharyngeal and vagus nerves
C. Right glossopharyngeal nerve only
D. Right vagus nerve only
E. Left glossopharyngeal nerve only
69. Vagus Nerve X
Sensations from skin at back of ear,
external acoustic meatus, part of
tympanic membrane, larynx, trachea,
espophagus, thoracic and abdominal
viscera
Sensations from bararoceptors and
chemoreceptors
Special sensory – taste from
epiglottis and pharynx
Somatic motor – Swallowing and
voice production via pharyngeal
muscles
Autonomic motor – smooth muscle of
abdominal viscera, visceral glands
secretions, relaxation of airways, and
normal or decreased heart rate.
Damage causes hoarseness or loss
of voice, impaired swallowing, GI
dysfunction, blood pressure
anomalies (with CN IX), fatal if both
are cut
70. Dyspnea
Dysphagia
Dysphonia
Dysarthria
Emotional liability if UMN
Total destruction incompatible with life
71. ACCESSORY NERVE (XI)
Cranial and spinal roots
Cranial roots: sternocleidomastoid (note
direction of head turn)
Spinal roots: trapezius (shoulder shrug)
72. Accessory Nerve IX
Swallowing, head, neck and shoulder movement via trapezius
and sternocleidomastoid and pharyngeal muscles
Damage causes impaired head, neck, shoulder movement
73.
74. It is purely motor. It has two roots, CRANIAL& SPINAL.
The spinal root arises from the anterior horn
cells of the upper 5 cervical segments, &it enter
the skull through foramen magnum.
These fibers are joined by the cranial root which arises
from the caudal part of the nucleus ambigus & together
they leave the skull through the jugular foramen with the
vagus.
In the jugular foramen the cranial root fibers join the
vagus to be distributed along with fibers of the vagus to
the pharynx and larynx.
This part of the nerve cannot be tested separately. The
spinal part supplies the sternomastoid and upper part of
the trapeziuz.
75. Hypoglossal Nerve XII
Tongue movements for speech, food
manipulation and swallowing
If both are damaged – can’t protrude tongue
If one side is damaged – tongue deviates towards
injured side
76. HYPOGLOSSAL NERVE
Movement of the tongue
Look for wasting and fasiculation of the
tongue
Deviation of tongue on protrusion
Tongue movements including power
77. Fibers arise from the medulla and exit the
skull via the hypoglossal canal
Innervates both extrinsic and intrinsic
muscles of the tongue, which contribute to
swallowing and speech
If damaged, difficulties in speech and
swallowing; inability to protrude tongue
78. Function of the Cranial Nerves
Olfactory (I) Smell
Optic (II) Vision
Oculomotor (III) Eye movement (Inf Rec/Med
Rec/ Sup Rec/Inf Oblique);
Focusing (Iris and Lens)
Trochlear (IV) Eye movement (Sup Oblique)
79. Function of the Cranial Nerves
Trigeminal (V) Chewing, sensation of scalp,
face, teeth (Not tongue)
Somatosensory information
(touch, pain) from the face and
head; muscles for chewing.
Abducens (VI) Eye Movement (Lat Rectus)
80. Function of the Cranial Nerves
Facial (VII) Taste (anterior 2/3 of tongue);
Somatosensory information
from ear; Controls muscles
used in facial expression.
Vestibulocochlear
(VIII)
Vestibular branch: Posture,
balance, equilibrium
Cochlear branch: Hearing
Glossopharyngeal
(IX)
Taste (posterior 1/3 of
tongue); Somatosensory
information from tongue,
tonsil, pharynx; Controls some
muscles used in swallowing.
81. Function of the Cranial Nerves
Vagus (X) Sensory, motor and autonomic
functions of viscera (glands,
digestion, heart rate)
Accessory (XI) Swallowing and head
movement (Trapezius and
SCM = Sternocleidomastoid
muscle)
Hypoglossal (XII) Controls muscles of tongue