This document discusses several topics related to sensory disturbances: 1) It describes the anatomy of the sensory system and how sensations are transmitted from receptors to the central nervous system. 2) It defines different types of sensory loss or disturbances like hypoesthesia, anesthesia, hypalgesia, and hyperpathia. 3) It outlines how to perform a sensory examination to localize lesions, including testing touch, proprioception, vibration, temperature, and pain. Higher cortical sensations can also be examined.

1. HEADACHE / DIZZINESS/
VERTIGO/ SENSORY
DISTURBANCE /SPHINCTER
DISTURBANCE
SRUTHI MEENAXSHI

2. CLASSIFICATION
As many as 90 percent of all primary headaches fall under a few categories, including migraine,
tension-type, and cluster headache.
While episodic tension-type headache (TTH) is the most frequent headache type in population-
based studies, migraine is the most common diagnosis in patients presenting to primary care
physicians with headache.

6. The mnemonic SNNOOP10 is a reminder of the danger signs ("red flags") for the presence of serious underlying disorders that can cause acute or
subacute headache :
●Systemic symptoms including fever
●Neoplasm history
●Neurologic deficit (including decreased consciousness)
●Onset is sudden or abrupt
●Older age (onset after age 50 years)
●Pattern change or recent onset of new headache
●Positional headache
●Precipitated by sneezing, coughing, or exercise
●Papilledema
●Progressive headache and atypical presentations
●Pregnancy or puerperium
●Painful eye with autonomic features
●Post-traumatic onset of headache
●Pathology of the immune system such as HIV
●Painkiller (analgesic) overuse (eg, medication overuse headache) or new drug at onset of headache

7. Giant cell (temporal) arteritis (GCA) is a chronic vasculitis of large and medium sized vessels.
The disease seldom occurs before age 50 years, and its incidence rises steadily thereafter.
A new type of headache occurs in two-thirds of affected individuals. The head pain tends to be
located over the temporal areas but can be frontal or occipital in location.
The headaches may be mild or severe.
Other common symptoms can include fever, fatigue, weight loss, jaw claudication, visual
symptoms, particularly transient monocular visual loss and diplopia, and symptoms of
polymyalgia rheumatica.
Laboratory testing may reveal an elevated erythrocyte sedimentation rate and/or serum C-
reactive protein, or thrombocytosis, but these are not specific.

8. The diagnosis of GCA is based on histopathology or imaging exams. Histopathologic evidence of
GCA is most often acquired by temporal artery biopsy.
Color Doppler ultrasound (CDUS) of the head, as performed by experienced operators, is an
alternative diagnostic procedure.
CDUS can visualize temporal artery abnormalities (eg, mural edema as shown by the "halo sign"
and "compression sign") characteristic of GCA.
When the diagnosis of GCA is still suspected in a patient who has had a negative temporal artery
biopsy and/or CDUS, the possibility of large vessel involvement can be evaluated by imaging the
torso with CT/CTA, MRI/MRA, or positron emission tomography (PET)

9. Trigeminal neuralgia
Trigeminal neuralgia is defined by sudden, usually unilateral, severe, brief, stabbing or
lancinating, recurrent episodes of pain in the distribution of one or more branches of the fifth
cranial (trigeminal) nerve.
The incidence increases gradually with age; most idiopathic cases begin after age 50 years.
Once the diagnosis is suspected on clinical grounds, it is important to search for secondary
causes.
Patients with suspected trigeminal neuralgia or those with recurrent attacks of pain limited to
one or more divisions of the trigeminal nerve and no obvious cause (eg, herpes zoster or
trigeminal nerve trauma) should undergo imaging to help distinguish classic trigeminal neuralgia
from secondary causes.
MRI and MRA of the head without and with contrast tailored to evaluate the trigeminal nerve is
the preferred imaging exam to evaluate for compression of the nerve by adjacent vessels or
other structures.

10. Chronic subdural hematoma may present with the insidious onset of headaches, light-
headedness, cognitive impairment, apathy, somnolence, and occasionally seizures. Imaging with
noncontrast CT or MRI is essential to confirm the diagnosis.
●Acute herpes zoster and postherpetic neuralgia often involve cervical and trigeminal nerves.
Pain is the most common symptom of zoster and approximately 75 percent of patients have
prodromal pain in the dermatome where the rash subsequently appears.
The major risk factors for postherpetic neuralgia are older age, greater acute pain, and greater
rash severity.
Acute herpes zoster is usually a clinical diagnosis based upon the characteristic vesicular lesions
in a restricted dermatomal pattern.
The diagnosis of postherpetic neuralgia is made when pain persists beyond four months in the
same distribution as a preceding documented episode of acute herpes zoster.

11. Brain tumor should be considered as a possible cause of new-onset headaches in adults over
age 50 years, as discussed above.

12. Dizziness
Dizziness" is a nonspecific term often used by patients to describe symptoms.
The most common disorders lumped under this term include vertigo, nonspecific "dizziness,"
disequilibrium, and presyncope.
The first step in the evaluation is to fit the patient with typical symptoms into one of these
categories.

13. VERTIGO
Vertigo is the predominant symptom that arises from an acute asymmetry of the vestibular
system.
The vestibular system includes the vestibular apparatus in the inner ear, the vestibular nerve
and nucleus within the medulla, as well as connections to and from the vestibular portions of
the cerebellum.

14. Distinguishing vertigo from other types of
dizziness
The spinning quality of vertiginous sensations is notoriously unreliable .
Lack of spinning cannot be used to exclude vestibular disease, given the difficulty many patients
have in putting their dizzy experience into words.
On the other hand, some patients with presyncope from vasovagal or cardiac disease can
interpret their sensation of dizziness as a spinning sensation

15. Distinguishing vertigo from other types of
dizziness
The spinning quality of vertiginous sensations is notoriously unreliable .
Lack of spinning cannot be used to exclude vestibular disease, given the difficulty many patients
have in putting their dizzy experience into words.
On the other hand, some patients with presyncope from vasovagal or cardiac disease can
interpret their sensation of dizziness as a spinning sensation .
The time course, provoking factors, and aggravating factors of dizziness are more useful features
in establishing the cause of dizziness.
One study found that many physicians that evaluate patients with dizziness may rely too heavily
on symptom quality for diagnosis and do not appreciate the clinical significance of these other
features .

16. Time course — Vertigo is never continuous for more than a few weeks. Even when the vestibular
lesion is permanent, the central nervous system adapts to the defect so that vertigo subsides
over several weeks.
Constant dizziness lasting months is usually psychogenic, not vestibular. However, the physician
must be clear on what a patient means by "constant."
Some patients who say they have constant dizziness for months actually mean that they have a
constant susceptibility to frequent episodic dizziness; this can be a vestibular problem.
A useful categorization divides patients with vertigo into those with acute prolonged severe
vertigo (eg, vestibular neuronitis, stroke), recurrent spontaneous attacks (eg, Meniere disease,
vestibular migraine), recurrent positionally triggered attacks (benign paroxysmal positional
vertigo), and chronic persistent dizziness (eg, psychogenic, cerebellar ataxia)

17. Aggravating factors — All vertigo is made worse by moving the head. This is a useful feature for
distinguishing vertigo from other forms of dizziness.
Many patients in the midst of a vertiginous attack are petrified to move. If head motion does not
worsen the feeling, it is probably another type of dizziness.

18. Associated signs and symptoms — Vertigo, whether of central or peripheral origin, is generally
accompanied by nystagmus and postural instability.
Other signs and symptoms may be useful in distinguishing between central and peripheral
causes of vertigo.

19. Nystagmus — The presence of nystagmus suggests that dizziness is vertigo.
Nystagmus is not always readily visible, although more subtle forms can be seen during
funduscopy or on electronystagmography. Some types of nystagmus are only seen after a
provocative maneuver (eg, Dix-Hallpike maneuver).
The bilaterally symmetric appearance of a few beats of horizontal nystagmus on lateral gaze is
normal (physiologic "endpoint" nystagmus).
Pathologic nystagmus is asymmetric or more pronounced or prolonged.
Certain features of nystagmus may suggest a central versus a peripheral cause of vertigo

21. CONTROL OF MICTURITION
1) CORTICAL MICTURITION CENTRE
2) PONTINE MICTURITION CENTRE
3) SPINAL MICTURITION CENTRE (SYMPATHETIC T11-L2 /PS S2/S3/S4)
4) PERIPHERAL NERVES (S2,S3,S4)

23. CORTICAL MICTURITION CENTER (CMC)
LOCATION: Paracentral lobule in the medial aspect of the Frontoparietal cortex
Function : Inhibitory to PMC
Dysfunction :Loss of social control of bladder
The brains control of PMC is part of social training in children experience at age 2-4 years

24. PONTINE MICTURITION CENTRE
(Also called as Barrington’s Nucleus)
Lateral region : Function : continence ,storage urine
Stimulation results in a powerful contraction of the urethral sphincter
Medical region : Function : Micturition centre
Stimulation results in decrease in uretheral pressure and silence of pelvic floor EMG signal,
followed by rise in detrusor pressure

25. SACRAL REFLEX OR SACRAL/PRIMITIVE
MICTURITION CENTRE (SMC/PMC)
1) Sacral parasympathetic nucleus (pelvic splanchnic nerves S2S3S4 NERVI ERIGENTIS )
2) Somatic –onufoid nucleus – collection of uretheral sphincter motorneurons
3) Levator animotorneurons

26. UNINHIBTED BLADDER
Lesion affecting the 2nd frontal gyrus and pathways leading from it down to pontine center
Frontal lobe tumours ,parassaggital meningiomas ,anterior communicating artery aneurysms , NPH
,parkinsons disease , multisystem atrophy
Features :
Urgency at low bladder volumes (detrusor hyperreflexia)
Sudden uncontrollable evacuation
NO residual urine
IF severe intellectual deterioration occurs urine may be passed at random without appropriate
concern

27. SPINAL BLADDER
Damage to spinal cord by trauma/tumour / multiple sclerosis
Fullness not appreciated
Intravesical pressure may only be indicated by sweating, pallor, flexor spasms, dramatic rise in
BP
Reflex emptying without warning
Incomplete evacuation may improve with practice and may be performed at will if massaged
and suprapubic pressure is applied
Detrusor – Sphincter dyssynergia
Evidence of Bilateral pyramidal lesion - enhanced reflexes and extensor plantar response
Bladder is small and contracted can hold maximum – 250 ml

28. AUTONOMOUS BLADDER ( Subsacral
lesion)
Damage to sensory and motor components in cauda eqina or pelvis
Cauda equina lesions, pelvic surgeries ,pelvic malignant lesions ,spina bifida ,high lumbar disc
lesions
MRI or myelogram is obligatory to exclude high disc lesions
Features :
Continual dribbling incontinence
Considerable residual urine with high infection risk
No sensation of bladder fullness – Large atonic bladder
May be associated with perineal numbness and loss of sexual function

29. SENSORY BLADDER
Similar to autonomous bladder
Anatomical explanation is uncertain
Primary problem is sensory denervation
Ultimately overdistension ,myogenic damage and contractile failure
Rare disorders: Tabes dorsalis , SACD , MS, Diabetes mellitus
Features : Massive retention of urine in litres – high risk of infection
Dribbling incontinence of sufficiently large volumes
Voiding possible with considerable straining but evacuation is incomplete

30. MOTOR PARALYTIC
Areflexic detrusor
-Marked by painful distension
-Inability to initiate urination
-Difficulty initiating urination ,straining and decreased size and force of stream, interrupted
stream and recurrent UTI

31. Sensory disturbance
ANATOMY OF THE SENSORY SYSTEM
Perception of a somatic sensation depends on detection of a stimulus by specialized receptors in
the skin, muscle, or joints.
Information from these receptors is then transmitted via peripheral nerves to the central
nervous system.
With the exception of the mesencephalic nucleus, whose projections carry proprioceptive
information from the muscles of mastication, the cell bodies of the primary sensory neurons
that constitute the peripheral nerves reside in ganglia outside of the central nervous system.
Projections from these ganglia then enter the central nervous system to synapse with second-
order neurons

32. The peripheral nerves are made up of large myelinated fibers that transmit proprioceptive, vibratory,
pressure, and touch stimuli, and small, poorly myelinated fibers that transmit pain, temperature, and
touch stimuli.
Note that touch is transmitted by both large and small fibers.)
Projections from the cell bodies receiving pain, temperature, and touch stimuli enter the spinal cord
via the dorsal nerve root.
These fibers terminate in the dorsal horns, fanning out over several segments . They synapse with the
second-order neurons in the dorsal horns.
These neurons then cross the midline of the cord in the anterior commissure in front of the central
canal, and these second-order neurons ascend (now on the opposite side of the spinal cord to the
peripheral nerve) in either the anterior spinothalamic tract (touch) or the lateral spinothalamic tract
(pain and temperature) to the ventral posterolateral nucleus of the thalamus.
Here, they synapse with neurons that ascend to the primary sensory cortex in the parietal lobe

33. Projections from the dorsal root ganglia (DRG) that carry proprioceptive, vibratory, pressure, and
touch stimuli directly enter the dorsal columns from the dorsal roots.
The gracile column is medial and carries stimuli from the lumbar and thoracic region; the
cuneate column begins laterally in the cervical region, which it subserves.
Thus, the dorsal columns consist of first-order neurons traveling ipsilateral to the peripheral
nerve from which they originate.
These neurons synapse with second-order neurons in the cuneate and gracile nuclei of the
medulla.
These second-order neurons cross in the dorsal midline of the medulla and ascend through the
brainstem as the medial lemniscus to the ventral posterolateral nucleus of the thalamus where
they synapse with third-order neurons that project through the internal capsule and the
centrum semiovale to the primary sensory cortex in the parietal lobe

34. DEFINITIONS
Sensory loss is categorized as follows:
●Hypoesthesia is the diminished ability to perceive pain, temperature, touch, or vibration.
●Anesthesia is the complete inability to perceive pain, temperature, touch, or vibration.
●Hypalgesia is the decreased sensitivity to painful stimuli.
●Analgesia is the complete insensitivity to painful stimuli.
Hyperpathia, hyperesthesia, and allodynia refer to an increased sensitivity to sensory stimuli.

35. SENSORY EXAMINATION
The goal of the sensory examination is to "localize the lesion.
This portion of the examination tends to be subjective because it relies on the patient's
responses to various stimuli; thus, it is usually done following the motor examination.
With the more objective data obtained from the motor examination, the examiner is often able
to narrow down a differential and proceed with a more focused sensory examination, resulting
in less frustration for both the patient and examiner.

36. The primary sensory modalities usually are examined first. These include touch, proprioception,
vibration, temperature, and pain.
Abnormalities in these sensations may occur with any sensory syndrome (eg, peripheral nerve
injury, radiculopathy, spinal cord syndromes, thalamic and cerebral hemispheric syndromes).
A disproportionate loss of vibration sense and proprioception, compared with pain and
temperature sensation, tends to occur with diseases of the dorsal columns of the spinal cord
(eg, tabes dorsalis, vitamin B12 deficiency, multiple sclerosis) and also with demyelinating
neuropathies and sensory neuronopathies.

37. Higher cortical sensation can be examined if touch sensation remains relatively preserved and the patient is suspected of having a cortical
lesion. Examination of cortical sensation includes two-point discrimination, graphesthesia, stereognosis, and extinction:
●Two-point discrimination is the ability to recognize two points applied simultaneously to the skin as distinct from a single point
●Graphesthesia is the ability of the patient to identify numbers or letters drawn in the palm of the hand.
●Stereognosis is the ability to recognize common objects such as keys, coins, or paper clips by touching or handling them with one's eyes
closed.
●Extinction is evaluated by simultaneously touching two separate points on either side of the body. The test is abnormal if the patient
consistently identifies the stimulus on only one side of the body. Extinction is seen in relatively large parietal lesions.
The Romberg is a test of proprioception.
It is positive when patients are able to stand with feet together and eyes open without losing their balance but are unable to remain
steady with the eyes closed.
This occurs because patients are using their eyes to compensate for the lack of sensory feedback they are receiving from their lower
extremities.
A functional correlate of this often comes out in the history when patients note that they lose their balance when they get up at night in a
darkened room.

39. The Sensory loss that is confined to a part of a limb suggests injury to a peripheral nerve, nerve plexus, or spinal
root (eg, mononeuropathy or radiculopathy). By contrast, sensory loss involving most of an extremity or the trunk
suggests the presence of other disorders, which may be distinguished as follows :
●Involvement of both sides of the body is consistent with a polyneuropathy or spinal cord disease, while
involvement of one side is consistent with contralateral disease of the brainstem, thalamus, or cerebral cortex.
●A sensory level is consistent with spinal cord disease or, more rarely, lateral medullary infarction.
●Sensory loss of the face can result from lesions in the upper cervical spine, brainstem, thalamus, or cerebral
hemispheres. With lower brainstem disease (eg, lateral medullary syndrome), the sensory loss on the face is
typically opposite that of the body, although ipsilateral sensory loss has also been reported ; sensory loss is on the
same side of the face and body with upper brainstem, thalamic, or hemispheric disease.
●"Stocking-glove" sensory loss is most commonly seen with length-dependent axonal neuropathies, although
other disorders may also present with this pattern.
●Disproportionate loss of vibration sense and proprioception, compared with pain and temperature sensation,
tends to occur with diseases of the dorsal columns of the spinal cord (eg, tabes dorsalis, vitamin B12 deficiency,
multiple sclerosis) and demyelinating polyneuropathy.

40. Thankyou