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Case Report | DOI: https://doi.org/10.31579/2642-973X/091
*Corresponding Author: Suresh. K, Family Physician & Public Health Consultant Bengaluru, India.
Citation: Suresh. K, (2024), Post- Non-Haemorrhagic Stroke Hypersensitivity - A Case Report and Brief Review, J. Brain and Neurological Disorders. 7(1): DOI: 10.31579/2642-973X/091
Copyright: © 2024, Suresh. K. This is an open-access article distributed under the terms of The Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 14 December 2023 | Accepted: 21 December 2023 | Published: 02 January 2024
Keywords: non-haemorrhagic stroke; central poststroke pain; thalamic pain; central pain; post-stroke thalamic pain; cerebral ischemia; right thalamus; right parietal; right temporal and occipital lobes infarct; neuroprotection
It is well documented that stroke patients seeking care in critical period recover almost fully from their paresis/paralysis, but minimal awareness is there about experiencing reduced and/or altered sensation because of stroke. After a stroke your sensation can be affected. The pathways from the brain to areas of the body are complicated and sensory problems are different for everyone. Sensory deficits include reduced or exacerbated ability to feel touch, pain, temperature, position, or the ability to recognise objects one is holding. Some people experience feelings such as tingling, prickling, numbness, aching, burning or ‘pins and needles. With altered sensation, movements may lack precision and control or even blow of air (direct or Coolers or Air conditioners) may appear painful.
Sensory re-education may have to be used to retrain or stimulate sensory pathways, through touching different textured objects, massage, vibration, pressure, determining joint position, identifying different temperatures. Sensory re-education can start from day one post stroke. Commonly recommended first- and second lines of pharmacotherapies like antidepressants, anticonvulsants, opioid analgesics, and lamotrigine, are more effective than others. Nonpharmacological interventions, such as transcranial magnetic or direct current brain stimulations, vestibular caloric stimulation, epidural motor cortex stimulation, and deep brain stimulation, are recommended in the management of therapy-resistant PS-TP. Interestingly, the stimulation to other areas, e.g., the motor cortex, periventricular / periaqueductal grey matter, and thalamus/internal capsule, show more effect than the stimulation to the thalamus alone. This article is based on Post stroke hypersensitivity case being managed currently and review of available literature and management practices.
Material & Methods: This article is based on case study a 51-year male software engineer, diabetic and hypertensive, having stroke in Mid-September 2023, who started getting sensory shock with fine touch of filaments of cloths since Mid-October 2023. He had non-Haemorrhagic infarct in the Right Thalamus, Right Parietal, temporal and Occipital lobes. Currently he is managing with exercises, relaxation methods like Meditation. Therapy with tapering cortisone has been suggested but not yet started.
It is well documented that stroke patients seeking care in critical period recover almost fully from their motor functions like paresis/paralysis (Hemiplegia or Paraplegia), but minimal awareness is there about experiencing reduced and/or altered sensation because of stroke. Up to 80% of people who have a stroke experience sensory loss in their affected arm. This sensory loss puts the arm at risk for injury and impacts functional use of the arm and the survivors' level of independence during daily activities. Central imbalance, central disinhibition, central sensitization, other thalamic adaptative changes, and local inflammatory responses have been considered as its possible pathogenesis. There are very few studies and reports about recovery from sensory loss or hypersensitivity. Multiple interventions for upper limb sensory impairment after stroke are described but there is insufficient evidence to support or refute their effectiveness in improving sensory impairment, upper limb function, or participants' functional status & participation. Poststroke thalamic pain a type of central poststroke pain, has been a hurdle to improve the rehabilitation outcomes and quality of life after a stroke. Its prevalence has been reported in 10–25% of stroke survivors. Most of the patient’s failed to manage the pain and hypersensitivity effectively [4]. Despite the different pharmacotherapies and invasive interventions, the understanding about the effects of such interventions used to address such impairments is limited and there is a need for more well‐designed, better reported studies of sensory rehabilitation. [1,4].
A stroke occurs when blood flow in the brain is obstructed and brain cells are deprived of oxygen-rich blood, they begin to die and lose function. When brain cells are damaged after a stroke, that area of the brain has difficulty directing nerves and cells that control motor functions. A stroke damages the way the nerves control our muscles, leading to muscles contracting for long periods or going into spasm, which will be painful. As stroke occurs due to reduced perfusion to a brain region, resulting in death or temporary or permanent neurological deficits including hemiplegia, hemiparesis, numbness, loss of sensory and vibratory sensation, balance problems, ptosis, decreased reflexes, visual field defects, apraxia, and aphasia [2]. More than half of stroke survivors suffer from sensory impairments of their affected upper limb (UL), which are characterized by reduced sense of touch, temperature, proprioception, and pain [1,2, 3]. They tend to have trouble processing sensory receptors, leading to numbness in the limbs in people who have had a stroke. Since every stroke is different, everyone recovers at different rates.
While the Numbness, tingling starts from the tips of the fingers and toes, giving a feeling of slits, between fingers and toes, itchy, uncomfortable stinging and later spreading to the arms and legs. Numbness after a stroke is different from other types of anaesthesia because the problems originate in the brain, not the local tissues.
Every stroke is different, everyone recovers at different rates. While the motor deficit’s recovery is assessed using Brannstrom’s seven stages of stroke recovery, which are i) flaccidity, ii) spasticity appears, iii) spasticity increases, iv) spasticity decreases, v) complex movement combinations, vi) spasticity disappears, and vii) normal function returns. The best progress is indicated by becoming more Independent, can cross Legs, sleep more, find the need to compensate less with technique and Spastic Muscles are twitching [3].
Sensory loss (Numbness) recovery is done using Fugl-Meyer Assessment—upper extremity (FMA-UE) sensory section [5]. This measures light touch and proprioception of the UL after stroke. The score ranges from 0 to 4 points for each subtest with a maximum score of 8 points per hand. While the focus after stroke is often on recovery of neurologic function and reducing the risk of recurrence, the emergence of comorbid conditions like poststroke Central Post-Stroke Pain and chronic headache is often overlooked and undertreated. The overall prevalence suggests that approximately 14% of adult patients with ischemic stroke have headache at the time of or shortly following their stroke diagnosis.
Hypersensitivity after a stroke, is not a rare phenomenon, where after reduction in sensation (numbness) during the attack and first 3-4 weeks until the progresses get stabilized, sudden change may be observed and complained, when even a slight touch irritates or gives electrical stimulation to the patient along with the process of recovery of motor functions of the affected limbs. Studies have shown that mechanisms like apoptosis, necrosis, inflammation, immune modulation, and oxidative stress and mediators such as excitatory amino acids, nitric oxide, inflammatory mediators, neurotransmitters, reactive oxygen species, and withdrawal of trophic factors may lead to the development of the ischemic cascade of hypersensitivity. All these agents have been shown to improve neurological outcome after ischemic insult in experimental animals suggesting that these will aid in preventing long-term morbidity and mortality associated with ischemic stroke [1,2].
Biomarkers have recently begun to be used in clinical diagnosis of ischemic stroke, especially in the acute phase. It is still very difficult to identify specific biomarkers for a particular neuroreceptors, that trigger or affect pathological processes in ischemic stroke and the mechanism underlying each receptor's involvement in the disease's development is not yet fully understood. However, target-based drug design and discovery for treatment of ischemic stroke could be a good starting point to work on addressing hypersensitivity too!
Pain is common after stroke, with an estimated 30 to 40% of stroke patients experiencing some form of pain. If person is recovering from stroke and experiencing pain, it’s important to first understand the underlying cause of the pain. Stroke patients can be encouraged to practice coping techniques at home also.
Case of Ravi who developed hypersensitivity after 4 weeks of Stroke:
Ravi, a 51-year male software engineer, stared getting sensory shock even with fine touch of filaments of cloths in Mid-October 2023. He had a stroke on the morning of 16 September 2023 after short period of a Parieto- occipital headache since the morning of 15/09/2023. His main complaint apart from hypersensitivity is feeling of left Upper extremity heavy. On physical examination his sensory appreciation of fine touch and temperature was highly exaggerated especially when these happened without his knowledge or him seeing. He scored 15 points (maximum=25) in Monofilament &18 points (maximum=36) in Shape and Texture test. Surprisingly firm holding of arm, pinching or pin prick did not bother him much.
History: A known hypertensive and diabetic over 15 years, measured BP at home which was 185/110, took some home Paracetamol tablet and rest. Next day too he had mild headache, therefore was resting most of the day. Around early morning of 16 September 0200AM midnight (16 &17 September midnight) headache increased, and he found left sided hemiparesis, that made the family to take him to an emergency admission in private Hospital, in Yeshwanthpur Bengaluru.
On admission the general examination recorded a Pulse rate of 98/minute, BP-215/88. The patient was conscious, well oriented, with left sided parathesis and numbness with reduced sensation, ataxia, and muscular strength of 4/5. Blood biomarkers down were 1) Hb1Ac=8.1% 2) Estimated average Blood sugar=186mg /Dl,3) Total Cholesterol=179, 4) Triglycerides=190, 5) HDL Cholesterol=36 mg/Dl, 6) LDL Cholesterol=127 mg/Dl, 7) VLDL=38 mg/Dl 8) Serum B 12 level= 30pg/ml (as against180-900 normal) 9) Plasma Homocysteine = 47.57mic.mol/L 10) Serum LFT biomarkers were all in normal limits. Pulmonary function test showed mild restriction. An MRI brain showed right territory acute infarct. MRA showed right vertebral artery occlusion and an old right MC A-ACA watershed infarct.
He was treated with dual antiplatelets, Statins and physiotherapy. At the time of discharge on 20/09/23 his BP was fully stables, left hemi-sided sensory loss with left sided ataxia. He was advised to take i) Ecosprin 150mg once in the afternoon) Clopilet 75 mg 1 tab in the afternoon iii)Rozat (Statin) tablet 20 mg in the night iv) Tab Homin ( for treatment of deficiency of vitamin B6, B9, & B12) 1 at in the morning and night, v) Tab. Trivolib2 (combination of Glimepiride, Metformin and Voglibose) one tab in the morning, vi) Novomix 30 Flexpen 100IU/ml - 1mg, 12 units a day, vii) Tazloc 40mg (anti-hypertensive) in the morning.
Diagnosis:
His involvement in ISCON’s Bhajans (chanting Hare Krishan, Hare Krishan, Krishna Krishna Hare Hare, Hare Ram, Hare Ram, Ram Ram Hare Hare, and Meditation has helped him to cope with hypersensitivity in the last 2 weeks.
Stroke recovery takes a toll on mental health. Experiencing pain or hypersensitivity in recovery adds to stress level and increase sensitivity. More than half of stroke survivors suffer from sensory impairments of their affected upper limb (UL) initially, which are characterized by reduced sense of touch, temperature, proprioception, and pain, but as the sensory recovery begins spontaneously on its own, sometimes with hypersensitivity within the first few months of recovery. Sensory impairments significantly limit the ability to use the upper limb after stroke. Like the loss of motor function in limbs (Hemi paresis) after a stroke, numbness occurs because the part of the brain that controls that limb has been damaged, and the brain works to compensate for the lost signal, or even send mixed signals. People experience many different types of sensations during this process, depending on where and how much the stroke has occurred. Two brain regions that determine post-stroke numbness or hypersensitivity are: thalamus and occipital lobe. The thalamus is responsible for 98% of all sensory input and the occipital lobe distinguishes this input from the five senses, including touch. Therefore, post-stroke numbness is often seen after a hippocampal or occipital stroke because these brain regions play a large role in sensory function [6].
Figure: 1. (a) Anatomical and (b) functional classification of the thalamus
Source: The role of thalamus. Mult. Scler. J. 2019; 26:6–16.
There are four types of sensory deficits reported [3,4]:
Monitoring the Progress: Sensory recovery is assessed by following tests [2,6]:
Semmes-Weinstein monofilament: This is to assess touch detection thresholds of the hand and fingers. The short version with five filaments from 0.07 to 279 g are used. The touch detection thresholds are scored on a 0 to 5-point scale, where 5 represents the thinnest filament and 0 represents the largest filament. Five different positions of the hand are tested: the fingertip on digits I, II, and V and the thenar and hypothenar regions, yielding a total sum score of 25 points.
Secondary outcome measures:
Treatment: Here are some treatments used for central neuropathy/central poststroke pain:
It is well documented that stroke patients seeking care in critical period recover almost fully from their motor functions like paresis/paralysis (Hemiplegia or Paraplegia).
There is minimal awareness about experiencing altered sensation because of stroke.
Multiple interventions for upper limb sensory impairment after stroke are described but there is insufficient evidence to support or refute their effectiveness in improving sensory impairment and upper limb function.
Sensory re-education, relaxation methods often help. Medical treatment of acute or subacute hypersensitivity is dependent on oral corticosteroids therapy.
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