Pattern Of Sensory Loss Research Articles

SENSE-Cog Lewy: Investigating the Impact of Sensory Loss on the Diagnosis, Clinical Features and Prognosis of Lewy Body Dementia

Abstract Background Lewy Body Dementia (LBD) accounts for 20% of the nearly 65,000 people with dementia in Ireland, but fewer than 5% of those affected receive a formal diagnosis. LBD includes both Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) and can be characterised by fluctuating and progressive cognitive difficulties, vivid visual hallucinations and REM sleep behaviour disturbances. Sensory function such hearing, vision and olfactory function declines with age—but increasing evidence shows that abnormal patterns of sensory dysfunction can be one of the earliest clinical signs and predictors of progression of neurodegenerative diseases such as Lewy body dementia and Parkinson’s disease dementia. Methods A scoping review was undertaken using Embase, CINAHL, PsychINFO and PubMed. Only reports on people with LBD (DLB and PDD) from any stage, prodromal to late stage were considered. Papers primarily addressing other forms of neurocognitive disorders were excluded. Sensory loss was conceptualised as the loss of smell, vision and hearing. Two reviewers independently assessed each study for inclusion, and disagreements were resolved by a third reviewer. Results Reports on sensory loss in LBD were very few and most often were comparing sensory loss across different dementia types. Strong associations were observed between olfactory loss and particular visual impairment patterns and the severity of both cognitive and non-cognitive DLB symptoms. Olfactory impairment is a potential early biomarker of DLB and PDD and severity of olfactory dysfunction can predict cognitive decline. Visual hallucinations, for example, were found to be closely linked to visual impairment patterns such as pareidolia. Conclusion This study highlights a knowledge gap regarding the patterns of sensory loss in LBD and their relationship with cognitive and non-cognitive LBD symptoms. Sensory assessments represent potentially valuable diagnostic and prognosis tool in LBD, with further research required to understand the aetiological mechanisms underlying sensory impairment in LBD and other dementias.

Unilateral ‘Ophthalmic nerve pattern’ of sensory loss from a demyelinating lesion in lateral cervical cord: a lesson in neuroanatomy (P14-3.002)

<h3>Objective:</h3> To describe an unusual localization for ‘ophthalmic nerve pattern’ of sensory loss and to review neuro-anatomic pathways of facial sensation. <h3>Background:</h3> Isolated ophthalmic nerve sensory loss is usually due to lesions in the ophthalmic nerve. Imaging of cervical spinal cord is not undertaken in patients with this finding even though spinal trigeminal nucleus (STN), which receives fibers that convey pain, temperature and light touch from the face and mucus membranes, extends from caudal pons to third/fourth cervical spinal cord level. <h3>Design/Methods:</h3> Case report. <h3>Results:</h3> A 54-year-old female with mild multiple sclerosis (MS) on no disease-modifying therapy (DMT), developed numbness and itching on her right scalp, radiating down her upper face. Neurologic exam revealed decreased sensation to light touch and pinprick in the distribution of the right ophthalmic branch (V1) and absent right corneal reflex. Vision, other facial sensation, cranial nerves and other neurologic functions were intact. Magnetic resonance imaging (MRI) of the brain revealed old demyelinating lesions and a new Gdenhancing lesion in the right side of the upper cervical cord, corresponding to the pars caudalis portion of the spinal trigeminal nucleus. She received gabapentin for pain, which was tapered as her symptoms resolved within weeks. <h3>Conclusions:</h3> Our patient appeared to have a lesion within the ophthalmic nerve, but her deficits were due to demyelination in pars caudalis of STN in cervical spine. Localized loss of sensation in our patient is likely due to somatotopic organization of STN whereby the midline facial structures are represented rostrally and the caudal portion – laterally (‘onionskin’ pattern). Patients presenting with unexplained ophthalmic nerve pattern of sensory loss may require dedicated imaging of cervical cord. <b>Disclosure:</b> Dr. Omari has nothing to disclose. Dr. Jain has nothing to disclose. Dr. Kister has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Genentech-Roche. The institution of Dr. Kister has received research support from Genentech. Dr. Kister has received publishing royalties from a publication relating to health care.

Trigeminal‐mediated headshaking: A diagnostic challenge

Trigeminal‐mediated headshaking: A diagnostic challenge

Myelopathy and polyneuropathy caused by nitrous oxide toxicity: a case report

A 19-year-old man presented with a 1-month history of progressive 4-limb numbness and gait imbalance. Physical examination revealed mild general muscular weakness, areflexia, and wide-based, ataxic, steppage gait. Sensory tests showed diminished superficial sensation below the level of the cervical-thoracic junction and a glove-and-stocking pattern of sensory loss at the 4 extremities. An initial magnetic resonance imaging examination of the cervical spine revealed an increased bilateral signal from the posterior and anterior columns on T2-weighted images. Nerve conduction velocity and electromyographic tests revealed polyneuropathy. On further inquiry, the patient admitted to chronic recreational use of nitrous oxide. The final diagnosis was nitrous oxide–induced neurotoxicity. The patient was treated for 5 days with injections of 1000 μg/day vitamin B12, followed by an additional 2-month treatment at a dose of 1000 μg/week. The numbness resolved after the first week, but there remained a mild sensory ataxic gait. The patient recovered fully after 2 months of treatment and nitrous oxide abstinence. We recommend an investigation of the patient's history of nitrous oxide exposure in cases where an individual presents to the emergency department or outpatient department with acute numbness characterized by megaloblastic red blood cells and symmetric neurologic deficits.

Altered pain and thermal sensation in subjects with isolated parietal and insular cortical lesions

Studies of sensory function following cortical lesions have often included lesions which multiple cortical, white matter, and thalamic structures. We now test the hypothesis that lesions anatomically constrained to particular insular and parietal structures and their subjacent white matter are associated with different patterns of sensory loss. Sensory loss was measured by quantitative sensory testing (QST), and evaluated statistically within patients relative to normal values. All seven subjects with insular and/or parietal lesions demonstrated thermal hypoesthesia, although the etiology of the lesions was heterogeneous. Cold and heat hypoalgesia were only found in the subject with the most extensive parietal and insular lesion, which occurred in utero. Cold allodynia occurred clinically and by thresholds in two subjects with isolated ischemic lesions of the posterior insular/retroinsular cortex, and by thresholds in two subjects with a lesion of parietal cortex with little or no insular involvement. Central pain occurred in the two subjects with clinical allodynia secondary to isolated lesions of the posterior insular/retroinsular cortex, which spared the anterior and posterior parietal cortex. These results suggest that nonpainful cold and heat sensations are jointly mediated by parietal and insular cortical structures so that lesions anywhere in this system may diminish sensitivity. In contrast, thermal pain is more robust requiring larger cortical lesions of these same structures to produce hypoalgesia. In addition, cold allodynia can result from restricted lesions that also produce thermal hypoesthesia, but not from all such lesions.

Assessment and Diagnosis of Sensory Disturbance

A patient may use various terms to describe sensory disturbance. Commonly used terms include numbness, pins and needles, tingling or pain. The actual area or pattern of sensory loss is more helpful in diagnosing the underlying cause, than focussing on the qualitative description of the sensory disturbance. Sensory disturbance can occur due to pathology anywhere along the sensory pathway: from the sensory cortex and deep white matter of the brain, through the spinal cord and nerve roots to the peripheral nerves ( Fig. 1 ). Assessment of paraesthesia therefore needs to be performed in an organized manner after a careful clinical history taking, which should guide the investigations in a focused direction to answer a specific question.

Symmetry of Sensory Loss in Developing Diabetic Sensory Polyneuropathy

The medical literature presents diabetic sensory polyneuropathy (DSPN) as an axonal length-dependent symmetric pathology producing a stocking-like pattern of anesthesia in the lower extremities. This has been based on anecdotal reports. Objective research has shown that damage may not occur in a purely length-dependent manner. A stocking distribution of sensory loss is atypical, and plantar sensory loss predominates. A single-blinded, age-matched, control/experimental study was performed of the symmetry of nerve damage in developing DSPN. Control (n = 46) and experimental (n = 83) subjects were examined. The patterns of sensory loss and the severity of axonal damage were evaluated. The right/left symmetry of pathology was recorded for each individual. Although there was not a stocking pattern of anesthesia found in developing DSPN, the pattern and severity of anesthesia were found to be generally symmetric. The severity of sensory impairment was symmetric at the dorsal foot (93%), lateral foot (95%), and plantar foot (69%). The most predominant site of sensory impairment was also symmetric (81%). This argues against a purely metabolic etiology for axonal damage. An anatomic component is implied. Further research will need to include examination of the unique physical characteristics of predominantly affected nerves.

The crossing of the spinothalamic tract.

The question whether the spinothalamic and spinoreticular fibres cross the cord transversely or diagonally was investigated in cases of anterolateral cordotomy and in a case of thrombosis of the anterior spinal artery. The pattern of sensory loss following transection of the anterolateral quadrant of the cord consists of a narrow area of decreased nociception and thermanalgesia at the level of the incision; it extends for 1-2 segments cranial and cordal to the incision. This area is immediately cranial to the area of total loss of these modalities. This pattern of sensory loss is explained as follows. The cordotomy incision transects two groups of fibres: those that are already within the anterior and anterolateral funiculi and those that are crossing the cord. The area of total thermanaesthesia and analgesia is due to transection of fibres that are already within this region. The area of partial sensory loss is due to transection of the fibres that are crossing the cord at that level. Owing to the craniocaudal extent of the branches of the dorsal roots, there is an overlap of their collaterals that results in every spinothalamic neurone receiving an input from several dorsal roots. The narrow cordotomy incision thus divides the few fibres crossing at that level, causing diminished noxious and thermal sensibility over a few segments above and below the incision. These facts can be accounted for only on the assumption that these spinothalamic fibres are crossing the cord transversely. This evidence of transverse crossing was found in the cervical, thoracic and lumbar segments. There were three of 63 cordotomies for which this explanation of the partial sensory loss could not be maintained. Although no explanation has been suggested, this is unlikely to be due to the fibres crossing the cord diagonally.

Pattern of Peripheral Deafferentation Predicts Reorganizational Limits in Adult Primate Somatosensory Cortex

Previous experiments have shown that the reorganization of the hand representations in areas 3b and 1 of somatosensory cortex of monkeys can be extensive or limited, depending on the pattern of peripheral sensory loss. After the loss of two or more digits, the deprived zones of cortex are not fully reactivated by remaining inputs from the hand (Merzenich et al., 1984). In contrast, after deafferentation of the entire glabrous surface of the hand, the deprived cortex becomes responsive throughout its extent to cutaneous stimulation of the dorsal hairy surface of the hand (Garraghty and Kaas, 1991). To test the hypothesis that it is the pattern of sensory loss and not the deprivation procedure that results in these differences, we mimicked multiple-digit amputation by deafferenting corresponding parts of the dorsal and ventral hand. We then recorded from areas 3b and 1 of 3 squirrel monkeys 3-11 months after the deafferentation. In each case, much of the cortex normally activated by the removed inputs remained unresponsive to cutaneous stimulation of skin surfaces of the hand with intact innervation. Thus, the reorganization that can occur in somatosensory cortex following peripheral sensory loss is constrained by the precise content of the stimulus deprivation; that is, there is a limit to the set of new receptive fields cortical neurons can acquire.

BENIGN HEREDITARY CEREBELLAR ATAXIA WITH EXTENSIVE THERMOANALGESIA

A New Zealand family with 3 members affected by late onset hereditary cerebellar ataxia is reported, distinguished by the development of near global thermoanalgesia. Because proprioception and autonomic function were preserved, and ataxia only slowly worsened, this proved to be a benign syndrome. The pattern of sensory loss indicated a 'length-dependent' neuropathy. Evaluation of sural nerve biopsy revealed a marked loss of axons, especially of those with diameters 1-7 microns and 0.2-1.5 microns. It therefore seemed likely that impairment of pain and temperature in the syndrome resulted from a loss of primary sensory afferents. It is concluded that this family represents a previously unrecognized variant and that the spectrum of hereditary ataxias needs to be widened to include an associated severe but selective loss of pain and temperature sensation.

Patterns of sensory loss following fractional posterior fossa Vth nerve section for trigeminal neuralgia.

Twenty-five patients with trigeminal neuralgia have been treated by fractional posterior fossa Vth nerve section. The procedure is shown to be effective in relieving pain, preserving corneal sensation and the motor root. Nineteen patients showed little loss of light touch sensation, and in 15 of these there was dissociation of sensory loss to pinprick and light touch. The results support the concept that there is some anatomical separation of fibres subserving light touch and pain in the posterior root of the nerve.

Diabetic Radiculoneuropathy: Clinical patterns of sensory loss and distal paresthesias

Diabetic Radiculoneuropathy: Clinical patterns of sensory loss and distal paresthesias

Temperature-linked sensory loss. A unique pattern in leprosy.

IN VIEW of the estimated 10 million 1 cases of leprosy in the world, and the virtually constant involvement of nerves, this disorder must be considered a most common disease of the peripheral nervous system. The cutaneous manifestations of the disease are variegated and well studied, but it is the involvement of the nervous system that results in the severe disabilities characterizing Hansen's disease. The motor deficits have been well described and are clearly related to a rather constant involvement of particular segments of certain nerve trunks. 2 Many of the resulting paralyses can be helped through tendon transfer surgery. Thus a hand may be returned to quite useful motor function, but sensory loss remains the immutable liability. With insensitive skin many of the activities of daily living may result in devastating trauma. The pattern of sensory loss in lepromatous leprosy has been described as either diffuse stocking-glove type