SENSORY ABNORMALITIES in diagnosis of neurological diseases

Sensory abnormalities

1. SENSORY ABNORMALITIES

2. SPINAL CORD Sensory afferent information passes through the dorsal root ganglia to the dorsal horn of the spinal cord. Some of the axons pass through the dorsal horn without synapsing and ascend in the ipsilateral dorsal columns; these serve mainly joint position and touch sensations . Other axons synapse in the dorsal horns, and the second-order sensory neurons cross in the anterior white commissure of the spinal cord to ascend in the contralateral spinothalamic tract for the conduction of pain and temperature information,

3. BRAINSTEM Axons from the nucleus gracilis and nucleus cuneatus cross in the medulla and ascend in the medial lemniscus . The spinothalamic tracts in the brainstem are continuations of the same tracts in the spinal cord and ascend lateral to the medial lemniscus in the brainstem.

4. THALAMUS The ventroposterior complex is the main somesthetic receiving area and includes the ventroposterior lateral nucleus, which receives information from the body, and the ventroposterior medial nucleus, which receives sensory input from the head and face. Projections are to the primary somatosensory cortex on the postcentral gyrus .

5. CORTEX - Sensory loss in the contralateral body is restricted to the portion of the homunculus affected by the lesion. Lesions of the postcentral gyrus produce more sensory symptoms than motor symptoms. Infarction of this region involving a branch of the middle cerebral artery can produce sensory loss with little or no motor loss More posterior lesions may spare the primary modalities of sensation (pain, temperature, touch, joint position) but instead impair higher sensory function, with manifestations such as graphesthesia , two-point discrimination, and the perception of double .

6. THALAMUS- Sensory symptoms in the contralateral body including the head & split at the midline. Sensory dysfunction without weakness is highly suggestive of a lesion of the thalamus. The thalamus receives vascular supply from the thalamoperforate arteries—which are branches of the posterior cerebral arteries often with some contribution from the posterior communicating arteries. In some patients, both thalami are supplied by one posterior cerebral artery, so bilateral thalamic infarction can develop from unilateral arterial occlusion .

7. SPINAL CORD- Sensory loss at or below segmental level, may be slightly different for each side. Motor examination is also key to localization. SPINAL CORD HEMISECTION- Sensory loss is ipsilateral for vibration and proprioception (dorsal columns) and contralateral for pain and temperature ( spinothalamic tract).

8. INTERNAL CAPSULE- Sensory symptoms in the contralateral body that usually involve head, arm, and leg to an equal extent NERVE ROOT/PLEXUS- Sensory symptoms follow a dermatomal distribution . Sensory symptoms span two or more adjacent root distributions , corresponding to the anatomy of plexus divisions PERIPHERAL NERVE- Distribution follows peripheral nerve anatomy or involves nerves symmetrically

9. NUMBNESS is the loss of sensation and usually manifests as decreased sensory discrimination and elevated sensory threshold; these are negative symptoms . DYSESTHESIA is an abnormal perception of a sensory stimulus, as when pressure produces a feeling of tingling or pain. If large-diameter axons are mainly involved, the perception is typically tingling; if small-diameter axons are involved, the perception is commonly pain.

10. SENSORY With a sensory level, loss of sensation in a myelopathic distribution without weakness and reflex abnormalities said to be very unusual . Sensory symptoms with incipient myelopathy are more often positive ; the Lhermitte sign is a common presentation of cervical myelopathy . A spinal cord localization is suspected with a sensory level , the level of the sensory loss may be slightly different between the two sides; this finding does not indicate a second lesion. T he evaluation of spinal sensory levels is to look for a lesion not only at the upper level of the deficit but also higher .

11. DISSOCIATIVE SENSORY LOSS Pain and temperature fibers cross shortly after entering the spinal cord and ascend contralaterally in the spinothalamic tract, whereas vibration and proprioception fibers ascend uncrossed in the dorsal columns. Therefore unilateral lesions of the spinal cord can produce loss of vibration and proprioception ipsilateral to the lesion and loss of pain and temperature sensation contralateral to it . This dissociation of sensory loss is most prominent in patients with intrinsic spinal cord lesions such as tumors, but it can also be seen with focal extrinsic compression .

12. A second form of dissociated sensory loss can arise from selective lesions of the dorsal or ventral aspects of the cord . Anterior spinal artery syndrome produces infarction of the ventral aspect of the cord, sparing the dorsal columns; therefore a deficit of pain and temperature sensation is found below the level of the lesion but vibration and proprioception are spared.

13. SUSPENDED SENSORY LOSS A third form of dissociated sensory loss is seen in syringomyelia , with loss of pain and temperature sensation, sparing of touch and joint-position sensation (usually affecting the upper limbs), and normal sensation above and below the lesion.

14. SACRAL SPARING Ascending spinal afferents are topographically organized , with caudal fibers peripheral to more rostral fibers. Therefore central cord lesions can affect the higher fibers before the lower fibers, so that sensory loss throughout the legs with sparing of perianal sensation may be found . In some patients with severe cord lesions , this preserved sensation may be the only neurological function below the level of the lesion.

15. BRAINSTEM Brainstem lesions uncommonly affect sensory function without affecting motor function. The notable exception is trigeminal neuralgia, characterized by lancinating pain without sensory loss in the distribution of a portion of the trigeminal nerve.

16. Lateral medullary syndrome typically results from occlusion of the posteroinferior cerebellar artery and produces sensory loss on the ipsilateral face plus loss of pain and temperature sensation on the contralateral body . With this syndrome, however, the motor findings eclipse the Sensory findings, which include ipsilateral cerebellar ataxia, bulbar weakness resulting in dysarthria and dysphagia , and Horner syndrome. Medial medullary syndrome typically results from occlusion of a branch of the vertebral artery and is less common than lateral medullary syndrome . Patients have loss of contralateral position and vibration sensation , but again, the motor findings predominate, including contralateral hemiparesis and ipsilateral paresis of the tongue.

17. Peripheral syndromes Polyneuropathy - The most common presenting complaint among patients with distal symmetrical peripheral polyneuropathy is sensory disturbance. The disturbance can be negative (decreased discrimination and increased threshold ) or positive (neuropathic pain, paresthesias , dysesthesias ) or both . Most neuropathies involve motor and sensory fibers, although the initial symptoms are usually sensory. Nerve conduction studies can evaluate the status of the myelin sheath , thereby identifying patients with predominantly demyelinating polyneuropathies , including AIDP & CIDP.

18. Diabetic Neuropathies Sensory involvement from diabetic neuropathy affects mainly small myelinated and unmyelinated axons, thereby producing disordered pain and temperature sensation. The findings often appear to be a paradox to the affected patient: loss of sensation yet with burning pain. The damaged axons cannot carry the patterns of action potentials, which accounts for the loss of sensation, yet spontaneous action potentials from damaged nerve endings plus increased susceptibility to discharge from mechanical stimuli cause the perceived neuropathic pain. Conventional neurodiagnostic testing often shows axonal neuropathy with sensory predominance.

19. Small-Fiber Neuropathy Small-fiber neuropathies (SFNs) typically present as a progressive burning pain , commonly seen first in the feet. Lancinating pain, numbness, and paresthesias along with symptoms of autonomic dysfunction are commonly seen . Examination demonstrates abnormalities of pinprick and temperature sensation in most patients.Vibratory perception is often affected. Reflexes are commonly normal.

20. Since sweat glands are innervated by small fiber nerves, quantitative sudomotor axon reflex tests (QSARTs) are highly specific and sensitive . Diabetes , autoimmune,paraneoplastic,vitamin deficiency/ toxicity,toxic metabolites,alcohol alcohol, heavy metals, and medications. Amyloidosis should also be considered , especially when it is accompanied by profound autonomic dysfunction .

21. Acquired Immunodeficiency Syndrome–Associated Neuropathies Human immunodeficiency virus type 1 (HIV-1) infection can produce a variety of neuropathic presentations. One of the most common is a painful , predominantly sensory polyneuropathy

22. Chemotherapy Some toxic neuropathies can be predominantly sensory. Such presentations are most commonly seen in patients with chemotherapyinduced peripheral neuropathy Although motor abnormalities do occur, the sensory symptoms eclipse the motor symptoms for most patients. Development of dyssesthesias , burning, and loss of sensation is the characteristic presentation. The neuropathy can be severe enough to be dose limiting for some patients and may continue to progress for months after the cessation of chemotherapy

23. AMYLOID NEUROPATHY Primary amyloidosis can produce a predominantly sensory neuropathy in approximately one-third of affected patients. Familial amyloid polyneuropathy is a dominantly inherited condition . Patients present with painful dysesthesias plus loss of pain and temperature sensation. Weakness develops later. Autonomic dysfunction is typical.

24. PROXIMAL SENSORY LOSS Proximal sensory loss involving the trunk and upper aspects of the arms and legs is uncommon but can be seen in patients with porphyria or diabetes and in some with proximal plexopathies with a restricted distribution . Other rare causes of proximal sensory loss include Tangier disease , Sjogren syndrome, and paraneoplastic syndrome . These neuropathic processes can be associated with pain in addition to the sensory loss.

25. Temperature dependent sensory loss Leprosy can produce sensory deficits that predominantly affect cooler regions of the skin, including the fingers, toes, nose, and ears. Temperature sensation is impaired initially, with subsequent involvement of pain and touch sensation in the cooler skin regions The deficit gradually ascends to warmer areas, typically in a stocking-glove distribution, with frequent trigeminal and ulnar nerve involvement.

26. AIDP Guillain-Barré syndrome, is an autoimmune process characterized by rapid progression of inflammatory demyelination of the nerve roots and peripheral nerves . Patients present with generalized weakness that may spread from the legs upward or occasionally from cranial motornerves downward . Sensory symptoms are generally are overshadowed by the motor loss

27. progressive weakness with areflexia . Nerve conduction studies can confirm slowing , especially proximally (F-waves are particularly affected). CSF analysis shows an increased protein level without a prominent cellular response ( albuminocytological dissociation).

28. CARPAL TUNNEL SYNDROME Compression of the median nerve at the wrist produces sensory loss on the palmar aspects of the first through the third digits . Motor symptoms and signs can develop with increasing severity of the mononeuropathy , but the sensory symptoms predominate , especially early in the course.

29. Nerve conduction studies usually show slowing of sensory and motor conduction of the median nerve through the carpal tunnel at the wrist. The slowing is present when conduction elsewhere is normal or at least Ulnar neuropathy Ulnar neuropathy is commonly due to compression in the region of the ulnar groove. Patients present with numbness in the ulnar two fingers (fourth and fifth digits). Weakness of the interossei develops with advanced ulnar neuropathy in any location , but sensory symptoms predominate, especially early in the course .

30. Motor nerve conduction studies show slowing of conduction across the elbow or wrist—the two common sites for ulnar nerve entrapment. Findings on sensory nerve conduction studies will also be abnormal if the lesion is at the wrist. EMG can show denervation in the ulnar -innervated intrinsic muscles of the hand.

31. Radial neuropathy. Radial neuropathy is often due to compression of the nerve in the spiral groove. Prototypically, this is seen in patients with alcohol intoxication, although cases are not confined to this in damage to muscles innervated distally to the triceps. Patients typically present with wrist drop, and sensory symptoms are minimal. Compression of the radial nerve distally in the forearm near the wrist can produce sensory loss and dysesthesias on the radial side of the dorsum of the hand; in this case there is no motor loss. The diagnosis is suspected clinically from the wrist drop in the absence of weakness of muscles of the arm innervated by other nerves.

32. Sensory findings, when present, are typical. Sensory findings in a radial nerve distribution without motor involvement suggest damage to the distal radial sensory nerve

33. Myelopathy Myelopathy typically produces sensory loss, although the motor and reflex findings eclipse the sensory findings in most patients. Nevertheless , when a patient presents with back pain with or without leg weakness, a sensory level should be sought. Some basic “pearls” regarding sensory testing A defined level is not expected. The sensory localisation is seldom complete which makes precize localisation difficult.

34. The sensory levels may not be same levels on both sides , a disceprency of upto several levels can be seen. There may be dissociated sensory loss due to uncrossed touch/ proprioception fibres vs crossed pain/temperature fibres . Disceprency in sensory levels between crossed spinothalamic levels can occur because of intersegmental projections of the axons of the posterolateral ( Lissauer ) tract . The sensory level may be much higher than might be expected from motor examination or pain. This is because the lesion may be much higher than indicated by the levels of clinical findings, reinforcing the basic precept that the examiner must start from the level of the symptoms and consider higher levels .

35. Syringomyelia Syringomyelia is the presence of a syrinx , or fluid-filled space, in the spinal cord that extends over several to many segments. This is most commonly associated with a Chiari malformation ( Koyanagi and Houkin , 2010). The mass effect of the syrinx produces damage to the fibers crossing in the anterior commissure that are destined for the spinothalamic tract, which conveys pain and temperature sensation. With more severe enlargement of the syrinx , damage to the surrounding ascending tracts may occur

36. HEMISECTION OF SPINAL CORD Below the level of the lesion, ipsilateral deficits in vibration and proprioception from dysfunction of the dorsal columns as well as contralateral deficits in pain and temperature from damage to the spinothalamic tracts are the characteristic findings. Ipsilateral weakness also is seen from damage to the corticospinal tracts.

37. SYPHILLIS - Tabes dorsalis is due to involvement of the dorsal roots by late neurosyphilis . Patients present with sensory ataxia, lightning pains, and often a slapping gait. Tendon reflexes are depressed. Trigeminal neuralgia- Trigeminal neuralgia is a painful condition that produces lancinating pain in the distribution of part of the trigeminal nerve. This is prototypical neuropathic pain . Patients have paroxysms of pain that usually last for seconds. Sensory loss does not occur, so its presence encourages further search for other diagnoses.

38. MENTAL NEUROPATHY Numb chin region may seem insignificant, it is often an ominous finding suggestive of an underlying and possibly undiagnosed malignancy. The diagnosis of a mental neuropathy warrants an aggressive malignancy evaluation . Nonmalignant etiologies include trauma and other jaw pathologies , multiple sclerosis, infections, connective tissue diseases, vasculitis , and sickle cell crisis