Wednesday, July 3, 2024

Iris Publishers-Open access Journal of Complementary & Alternative Medicine | Comprehensive Role of Otorhinolaryngologists in the Management of Headache: A Prospective Tertiary Care Centre Based Study

 


Authored by Rajwant Kaur Kamal*,

Abstract

Background: Headache is most common complaint of human being. Classified into primary (migraine, tension headache and trigeminal neuralgia) and secondary (infectious, vascular and drug induced). Sinugenic headache is deep seated, dull aching with fullness and heaviness in sinus area. The purpose of study to assess the comprehensive role of otorhinolaryngologists in the diagnosis of headache and to evaluate the efficacy of medical and surgical management of patients presented with headache. 200 patients reported to rhinology clinic with headache. Detailed history, head and neck examination routine blood investigation, fundus examination & anterior rhinoscopy, radiological investigations X-ray paranasal sinuses, skull & cervical spine and direct nasal endoscopy was and CT paranasal sinus preoperatively done.

Results: 200 patients assessed using VAS analog scale before and after treatment dividing into four groups: resolved, improved, no change, and worsened’ group; p value was statistically significant in resolved and improved group whereas non-significant in no change and worsened group. 129 patients had non-sinugenic headache; 29(22.48%) with cervical cause, Migraine 24 (18.60%) and ophthalmic 23 (17.48%) respectively; dental and vascular 19 (14.72%) each, and psychogenic headache in 13 (10.07%) and trigeminal neuralgia in 2 patients (1.55%). 96.12 % were relieved by medical treatment whereas 71 patients of sinugenic headache 21.12% were treated successfully with medical treatment. One refused surgery, 50/55 (90.90%). Improvement assessed by SNOTT-22 pre- and post-surgery that was statistically significant p value-0.002.

Conclusion: Headache need comprehensive management. Sinugenic headache managed successfully initially with medical treatment and refractory cases by surgical intervention with equal efficacy.

Keywords:Sinugenic headache; Otorhinolaryngologists; SNOTT-22; Contact point headache

Abbreviations:VAS score: Visual Analogue; SNOTT-22: Sino Nasal Outcome Test; BT: Bleeding time; CT: Clotting Time; CTPNS: Computed Tomography Scan Of Para Nasal Sinuses; HIS: International Headache Society; DNS: Deviated Nasal Septum

Background

Headache is very annoying, distressing, and common condition both for patient as well as physician. It is the second most common complaint with which patient present to general physician, otorhinolaryngologists, neurologist, othropaedician, ophthalmologist and psychiatrist [1]. Headache can be primary (migraine, tension or cluster headache and trigeminal neuralgia) or secondary (infectious, vascular and drug induced). Primary headache is often associated with gastrointestinal or sensory symptoms and effected by various environmental factor [2]. Another classification of headache is superficial and deep which is often helpful in locating the source of headache. Superficial pain is felt exactly at the site of insult and is of burning quality often associated with increase in blood pressure and movement, on the other hand deep pain also known to be referred pain is often dull aching in nature due to involvement of the muscle and blood vessel and often associated with hypotension or nausea and vomiting [3]. International Headache Society (IHS) and the American Academy of Otolaryngology- Head and Neck Surgery (AAO-HNS) described various conditions of sinugenic headache. Sinusitis pain comes from inflamed and engorged nasal structures like turbinate, nasofrontal ducts, Ostia and superior nasal spaces. Sinugenic headache is usually deep, dull aching with complaints of fullness and heaviness, and more during awakening, and seldom associated with nausea and vomiting. IHS classification place paranasal sinus disease in the etiology of headaches and facial pain in section 11.5 [4, 5]. The mechanism of type of headache effects the role of otorhinolaryngologist in identification, diagnosis, and treatment of the underlying causes. As the symptoms are overlapping for both sinugenic and non sinugenic headache or even exist simultaneously in the same patient more liberal diagnostic approach needed [6]. So, the present study done to assess the comprehensive role of otorhinolaryngologist in the management of headache (sinugenic and non sinugenic) and to evaluate the efficacy of medical and surgical treatment for sinugenic headache (Figure 1).

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Methods

The present study is a tertiary centre based prospective study on 200 patients reported to rhinology clinic during the time of June 2017-July 2018 with the complaints of headache along with other overlapping symptoms. Institutional ethical committee clearance has been obtained as it contain human participants. These patients came directly or were referred from other departments like ophthalmology, general medicine, neurology, orthopedic and psychiatry. Inclusion criteria are headache localized to the periorbital, frontal or zygomotemporal regions of more than 2 weeks duration with clinical feature suggestive of sinusitis (based on detailed history, systemic examination, ENT examination and investigations). Headache that improves with use of topical anesthesia mainly 4% lignocaine was used plus local nasal decongestant. Worsens with change in pressure like diving, flight or with climatic changes. So, following diagnostic criteria are included:

a) Headache usually recurrent, non-seasonal, and not associated with fever or localized tenderness in the region of sinuses and erythema.

b) Headache or facial pressure that developed simultaneously after acute onset or acute-on-chronic rhino sinusitis.

Exclusion criteria are patient having severe headache suggestive of intracranial disease or clinically other than sinugenic headache; not consenting to participate. Patients of age group above 10 years and less than 60 years of either sex were included in the study. All the patients suffering from headache for more than 2 weeks duration, mainly located in the frontal, malar, vertex, temporal and neck region. A thorough detailed history was taken with clinical and systemic examination done to rule out all possible causes such as hypertension, cluster and tension headache, migraine, neurological, ophthalmological, and various other causes. Detailed history of headache regarding its localization, mode of onset, duration, periodicity (continuous or intermittent), progressive or non-progressive, intensity of pain and its radiation, type of pain, any aggravating or relieving factors, duration of each attack as well as frequency, time of attack any associated symptoms of nausea and vomiting, and sinugenic causes like nasal obstruction, discharge, anosmia, epistaxis, sneezing etc. was taken (Figure 2).

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All the 200 patients referred to rhinology clinic with presumptive diagnosis of rhino sinusitis, were subjected to routine complete blood examination with BT, CT, urine for albumin, sugar and microscopic examination, and X-ray cervical spine both (anterio-posterior and lateral view) selectively in patients complaining of neck pain. All patients underwent anterior and posterior rhinoscopy, rigid digital nasal endoscopy examination under local anesthesia (4% lignocaine+nasal decongestant) with 0- and 30-degree endoscope, to assess the condition of nasal mucosa, nasal septum and conchae, nasopharyngeal end of Eustachian tube or nasopharynx, also to see any sign of draining mucous from the sinuses. When sinugenic cause were highly suspected then patient was subjected to radiological investigations in the form of X-ray paranasal sinuses water’s view but plain and contrast enhanced CT was only done, to evaluate for any anatomical variations other than normal. So once diagnosis was confirmed patients were advised surgery. MRI was done in selected cases having overlapping symptoms. Headache intensity was graded with 10-point visual analog scale (VAS) 0-10, here 0 signified absence of pain and 10 most intense pain. For further analysis, after post treatment patients were divided into four categories; ‘resolved’ group consisted of patients who rated headache that was almost completely resolved, ‘improved’ group (group I&II) was defined as patients who is after treatment VAS score was lower than they’re before treatment score, ‘no change’ group comprised patients who showed no change in the VAS score, and the ‘worsened’ group (group III&IV) included patients who’s after treatment. After treatment VAS score in sinugenic and non sinugenic patient were assessed 2 weeks, 1, 2, 3, 6 and 12 months in group I & II and III & IV.

Effectiveness was determined for management strategies. These were as follows:

1. Upfront medical therapy (when sinusitis was suspected). Those who were not responded and pinpointing the other aetiology were managed by combined effort of concerned specialties.

2. Upfront surgical management guided by CT scan of paranasal sinus.

Sinonasal-Nasal Outcome Test (SNOT-22) questionnaire was used to assess the improvement in patients who underwent surgery (pre and postoperatively after 6 months of surgery). Each item score was measured, and higher scores indicated worse symptom severity as follows: 0 = “no problem”; 1 = “very mild problem”; 2 = “mild or slight problem”; 3 = “moderate problem”; 4 = “severe problem”; and 5 = “problem as bad as it can be”.

Results

A prospective study was conducted on 200 patients complaining of headache reported to rhinology clinic during time interval of June 2017-December 2018 with complaints of headache and other overlapping symptoms. These patients came directly or referred from other specialties like ophthalmology, general medicine, neurology, othropaedician, and psychiatry. Patients above 10 and less than 60 years included with mean age 36.58 + 12.28. Majority of the non sinugenic patients fell in the 41-50 age group, followed by 31-40. Whereas sinugenic patients were more in 21-30 age group followed by 10-20 age group (Figure 3).

So, the most common cause of non-sinugenic headache was cervical pain among 29 (22.48%) patients including 13 male and 16 females mostly above 40 age group. Migraine and ophthalmic cause were other common cause of non sinugenic headache involving 24 (18.60%) and 23 (17.82%) patients, respectively. Migraine was more prevalent among female whereas ophthalmic cause was equally common in both sexes. Other causes were dental and vascular involving 19 (14.72%) number of patients of each cause whereas vascular cause was found mostly above 40 years next cause was psychogenic headache in 13 (10.07%) with slightly more predilection for female population. Other cause was trigeminal neuralgia involving 2(1.55%) patients (Table 1).

Table 1: Age and sex wise distribution of patients with non sinugenic headache (n=129).

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Table 2: Age and sex wise distribution of patient with sinugenic headache according to mucosal contact point. (n=71).

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Among 29 patients of cervical pain only 15 % exhibited osteophytes and osteoarthritis on the cervical region radiology rest having almost normal finding, pain was significantly relieved by taking analgesic and physiotherapy as advised by othropaedician. 23 patients of the ophthalmic cause, 20 had refraction error and after correction they had significant improvement, 2 had papilledema (due to retinal hemorrhage) included in resolved and improved group, only one among them had no relief due to associated myopathy included in group III. Rest 13 patients referred to neurologist to rule out any organic cause and after all the necessary investigation and examination when no specific etiology was found referred to psychiatrist. After treatment only 7 patients were completely relieved of their headache 4 patients had partial relief whereas 1 patient with slight improvement in symptoms (12 patient in resolved and improved category of VAS) and 1 patient had no relief at all. Migraine disorder in 24 patients were found to be more common in the age group 21-30, followed by 31-40 with female preponderance and almost all the patients were benefited by ergot preparation except 1 patient who was having associated allergic rhinitis. Dental and vascular causes were treated according to their causes with significant relief of pain. One female patient of trigeminal neuralgia was relieved successfully with medical management whereas the male patient had worsening of symptom referred to neurologist.

All the 71 patients of sinugenic headache and its symptoms underwent nasal endoscopy and CT PNS. As in that pain was drastically improved using local anesthesia and nasal decongestant. Based on endoscopic examination and CT scan DNS (36.61%), DNS with allergic rhinitis (16.90%), osteomata complex disease (14.08%), nasal polyp (11.26%), allergic rhinitis (18.30%), and atrophic rhinitis (2.81%) were detected. (Table 2) The preoperative mean Lund Mackay score was 9.75.

Septoplasty was done for DNS or DNS with spur. According to the presence of mucosal contact point on diagnosis, functional endoscopic sinus surgery including middle turbinectomy, ungiectomy, and ethmoidectomy like procedure were done with no adverse event during the procedure, so postoperative was 10.309 which was statistically significant (p 0.002 value) (Table 2).

Age and sex distribution (sinugenic causes) 13 patients of allergic rhinitis and 2 patients of atrophic rhinitis were treated medically, only 8 patients among allergic rhinitis had significant improvement but the rest 5 had partial relief. Medical treatment was given in form of topical nasal decongestant, topical and oral corticosteroid, in active cases antibiotics (macrolides) were added. Initially it was given for 2 weeks then for 1, 2, and 3 months depending upon the patient response. Other 56 patients one patient refused for surgery, rest 55 after medical fitness. An informed consent underwent surgery including septoplasty, middle turbinectomy, uncinectomy, and ethmoidectomy according to the anatomic variation. Overall success rate of the surgery in relieving headaches was measured by using SNOTT-22 score which represents the most validated and widely utilized measure for chronic rhinosinusitis [7]. Headache was completely relieved in 31 (56%) patients, 19 (35%) patients reported a decrease in the headache intensity whereas in 4 (7%) patients it remained unchanged and 1 (2%) patient had worsening of headache intensity. Pre- and post-operative (after 6 months) scores were analyzed and found to have significant correlation (preoperative SNOTT 22 was 17.145 and postoperative was 10.309 which was statistically significant, p <0.002 value).

Discussion

Sinugenic headache is often associated with significant morbidity and remains a challenge for both clinician and patient and mostly diagnosed by exclusion. As sinugenic headache patient may have multifactorial etiology and comorbities, so these patients always challenging to manage, and mostly require the interdisciplinary care to achieve good result. 8 The present study evaluated the comprehensive role of otorhinolaryngologist along with other concerned specialties for the management of headache. And at same time the efficacy of medical and surgical treatment was assessed without much difference if sinugenic and non-sinugenic headache was rightly diagnosed. Currently ‘contact point headache’ is more highlighted than the classic entities of acute and chronic rhinitis as a primary cause of sinugenic headache. It is a syndrome secondary to mucosal contact points that can be deviated nasal septum (DNS), DNS with septal spurs, concha bullosa, hypertrophied inferior turbinate, uncinated bulla, medialized or paradoxical middle turbinate and large ethmoidal bulla in the Sino nasal cavities may be without any sign of inflammation, hyperplastic mucosa, purulent discharge, and sinonasal polyps or masses. Sinugenic entities like sinusitis sometimes mimics or precipitate neurogenic syndromes. As it is common in sphenoid sinusitis. It may cause visual disturbance, or cranial neuropathy [9]. Many studies suggest that surgical removal of such mucosal contact points is more effective than medical therapy to improve quality of life [10, 11]. In present study 200 patients were enrolled with chief complaint of headache. Out of these 200, 129 (64.5%) were categorized as non sinugenic cause and rest 71 (35.5%) sinugenic cause of headache after thorough history taking and complete head and neck examination, and nasal endoscopy after local anesthesia. Among non sinugenic headache, major cause was cervical pain (29), followed by migraine (24), ophthalmic cause (23), vascular (19), and psychogenic headache (13). Similar study conducted by Foroughi pour et al., in 2011, studied 58 patients presented with sinugenic headache. All patients were assessed for 6 months by otorhinolaryngologist and neurologist, and finally diagnosed with migraine (68%), tension-type headache (27%), and chronic sinusitis with recurrent acute episodes in (5%) of the patients [12].

Yet another study done by Eross et al in 2007 found that among 100 self-diagnosed headache patients in primary care and general population, migraine remain the most common diagnosis in 52%, only 3% had sinugenic headache and 9% had non classifiable headache. Most common reason for misdiagnosis may be headache location, associated and aggravating features [13]. Similar study conducted by Kumar KS et al in 2019 suggested prevalence of sinugenic headache in 13% whereas migraine in 53% and tension headache in 31% [14]. Yet another study conducted by Debdulal Chakraborty et al in 2018 had 98 patients of sinugenic headache out of 200. Among sinugenic patient’s majority of them had DNS (40.81%) or osteomeatal complex disease (34.69%) followed by nasal polyps (12.25%) and allergic rhinitis (8.17%) [15]. In the present study, among 71 patients of sinugenic headache DNS (36.61%), DNS with allergic rhinitis (16.90%), osteomeatal complex disease (14.08%), nasal polyp (11.26%), allergic rhinitis (18.30%), and atrophic rhinitis (2.81%) were detected, with highest incidence among 21-30 years followed by 11-20 years. Similarly, in the study conducted by Pramod Kumar et al. majority of the headache cases were seen in the 10-30 years [16]. In most of the patients had headache localized to forehead, periorbital area followed by glabella, malar area, and with more than one site. The mean headache frequency was 4 episodes per month and mean headache severity was 1.5 hours. The average initial onset of headaches was 18 months, ranging from 2 weeks to 8 years. Post treatment patients were assessed using VAS analogue scale and divided into four groups; resolved group, improved, no change group, and worsened group. Present study suggested that VAS score was statistically significant in group I& II in both non sinugenic and sinugenic patients whereas it was not significant in group III & IV. That result was very much like the study done by Wee et al, in 2015 on characteristic of rhinogenic headache which noted statistically significant VAS score in group I &II and non-significant in group III& IV in pre- and post-operative patients with sinugenic headache [17].

Our study suggested that 129 patients of non sinugenic headache 96.12 % were relieved of their headache successfully by otorhinolaryngologist in collaboration with other specialties. These patients initially had sign and symptoms of sinusitis, which was managed with topical decongestant, topical or oral steroids, but due to others overlapping symptoms concerned with relative specialty. So, with proper diagnosis most of the non-sinugenic headache patients were managed successfully. Among 71 patients of sinugenic headache 21.12% were treated successfully with medical regime for minimum of 3 months in form of local corticosteroid, whereas in acute and active stage macrolides antibiotics along with oral corticosteroid (only when indicated), whereas rest 56 patients who were refractory to medical treatment were advised surgery. Among them one patient refused to give consent for surgery. 50/55(90.90%) patients had significant improvement assessed using SNOTT-22 score 6 months after surgery. Whereas overall surgical success rate was only 80% in Wee et al study. Similar study conducted by Willatt and Low suggested 63% relieved in intensity of chronic headache [18]. But Parsons and Batra studied that 91% had relief in intensity of sinugenic headache after FESS [19]. Similarly, Clerico et al. noted 79% of improvement in sinugenic headache not only in severity but also in intensity [20]. On the other hand, Ragbad et al found significant objective and subjective improvement in management of headache without any difference between the line of treatment either medical or surgical. That was in accordance with present study as patients with sinugenic headache were first treated on medical line and only refractory cases and patient with contact point headache were taken up for the surgery with significant improvement in intensity and frequency of headache [21]. Currently no data is available that suggest which line of treatment is superior to the other for the management of sinugenic origin of headache.

Conclusion

Headache is a symptom which is universally experienced by human being. Usually, these patients have multifactorial etiology. So, the present study suggested that initial medical regime followed by surgery in refractory cases were equally effective with little difference. Moreover, the present study management protocol was very fruitful and encouraging to reduce the cost of treatment and decreasing the psychological burden of surgery and its potential risk of its complication. Such patients require interdisciplinary care to overcome the challenges to manage them. A detailed history and thorough evaluation are required to rule out whether it is of sinugenic or non sinugenic origin. Sinugenic headache patients need radio logical assessment and nasal endoscopy to find the status of the paranasal sinuses and mucosal contact points. Non sinugenic patients can be managed with 96.12% success rate in collaboration with other specialties and all sinugenic patients firstly should be treated on medical line then only refractory cases should be considered for surgery with 90.90% success rate. A thorough diagnostic workup is required to find out the etiologies of headache and this is the main key in management of patients with sinugenic and non sinugenic headache. There are few limitations of present study firstly a small sample size and secondly short duration of follow up for assessment of management in VAS score especially in no change and worsened group. Despite these short comings present study management protocol will provide interest for the future aspirants to reinvestigate it, specially validating the less common causes of sinugenic headaches such as mucosal contact point.

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Iris Publishers-Open access Journal of Textile Science & Fashion Technology | The River Island Case Study: Implications for Differentiation and Re-Positioning

 


Authored by Arooj Rashid*,

Abstract

This article aims to examine fashion retail brands’ differentiation and re-positioning strategies using River Island as a case study. It hereby describes how structure of the fashion industry has been subject to evolutionary change since the early 2000s. It also shows that River Island was able to use its own brand strategy to take a unique position in the market, while also establishing an identity as an international wholesale brand identity through its exploration of several different channels.

Keywords:Fashion industry; Retail brand; River Island; Channel expansion

Introduction

Since being established in 1948 by Londoner Bernard Lewis, the fast-fashion retailer River Island has had three different names: Lewis Separates, Chelsea Girl, and River Island [1]. After occupying an unused site in London’s East End, where he sold knitting wool, Lewis partnered with three of his brothers, opening 70 Lewis Separates stores across the UK. Although it sold clothing typical of the 1950s, Lewis Separates gained renown for never carrying many of the same items, meaning the products were relatively unique. Lewis Separates also sold family clothing, meaning that young adults could shop in the same stores as their parents and buy the same styles [2]. Nonetheless, following the economic boom of the 1960s, Lewis Separates found that they had to shift from offering family-wear to be a boutique for the younger generation.

This shift, coupled with the increasing purchasing power of younger consumers, made the firm re-brand and re-position itself to ‘Chelsea Girl’, the name taken from King’s Road in Chelsea [2]. This was considered a suitable strategy at the time due to the rise of Chelsea as a pop culture and fashion icon. Chelsea Girl’s cheap yet cheerful image showed that Bernard understood the demands and expectations of the target market [3]. Consequently, the firm opened a menswear division in 1982, named Concept Man; not long after that, Chelsea Girl was finally re-branded to the current name River Island [3], influenced by the River Thames, close to where Bernard had lived, and his boat [4].

River Island has remained the brand name since the 1990s, and the firm continues to sell own-label products in its 250 UK stores. River Island utilizes a monolithic – also called branded house – strategy [5,6], enabling it to take on a unique position in the market. For example, the product categories are designed to be in line with the name and design of the retail stores [7].

While River Island continues to focus on selling its own-labelled products under its main brand name, it has recently developed and expanded, bringing in its Holloway Road line of menswear and reviving the Chelsea Girl label, this time as a sub-brand. Its Chelsea Girl launch was supported by Lucy Moller, a National College of Art and Design graduate who draws inspiration from the brand’s 60s, 70s, and 80s high street favorites [8]. Aiming to evoke a sense of nostalgia for consumers who shopped at Chelsea Girl in their youth, the products have a unique vintage style that echoes the brand’s early bohemian aesthetic. Finally, River Island also brought in the RI Baby collection for newborns in 2018.

Current Positioning and International Expansion

Beyond its product line expansion on a national scale, since 2010 River Island and other British fashion brands e.g. Barbour, Reiss, Jack Wills has also been exploring opportunities to expand internationally, initially going into partnership with ASOS to achieve worldwide recognition [9,10]. This represented a new direction for River Island in that it utilized a wholesale brand strategy, i.e. using other retailers to sell its own-label products. This partnership can be considered suitable due to the pure-play retailer’s increasing popularity in the USA, Germany, France, among others, in addition to the UK [9]. Once it had achieved its goal of global recognition, River Island continued its expansion in 2013 by engaging with international e-retailers, entering the German and Swedish markets through, e.g., Zalando.com. Retailers gain a key advantage in employing wholesale brand strategies with pureplay retailers, especially international e-tailers like ASOS, in that they can achieve international exposure for the brand, thereby promoting British heritage indirectly and enhancing the brand’s national image [11,12]. For instance, while a UK customer may not consider entering a River Island store, they may develop an interest in products from River Island while shopping on the ASOS website. Meanwhile, customers from other countries visiting an e-tailer’s website may identify River Island as a British fashion brand, as it is considered a foreign brand. This may be beneficial for the brand positioning as in many countries, Britain has an association with quality. Hence, by expanding to both national and international e-tailers, fashion retailers can go beyond improving their brand image on the national level to further strengthen their brand positioning and compete internationally [11]. River Island began to diversify its product brands in 2018 by selling other premium brand labels, both in its stores and through its online channels, such as Levi’s and Only & Sons. Finally, the fashion retailer launched Harpenne (owned by River Island Global Holdings) in 2019, continuing its market rise with a range exclusively targeting women 40 years old and above [13]. It reached this demographic by setting up a dedicated channel under the sub-brand. However, the crisis caused by the Covid-19 pandemic caused trading to stop soon after, and River Island shifted its focus to its current portfolio.

Re-positioning and differentiating

To offer customers an exclusive in-store experience while also enhancing its international positioning, River Island could draw inspiration from the approach of Boohoo.com, which launched a pop-up shop at the music festival in Coachella, USA. This emerged as a successful move as it allowed the value-led fast-fashion e-tailer Boohoo to set up a physical, albeit temporary, store to target younger adults with upmarket backgrounds, not to mention young celebrities. With its similar target market, River Island could also collaborate with international music festivals, thereby enhancing its national and international recognition. It stands to gain from establishing a pop-up store in such an environment as customers are able to have a tactile experience with the products during their purchase decision-making. A physical presence is especially beneficial in the current era, with customers still wary following Covid-19 lockdowns and restrictions yet also looking forward to going out again. In addition, another strategy going forward would be to reintroduce the Chelsea Girl label as a womenswear subbrand, nationally and internationally, thereby attracting consumers who remember shopping there. Specifically, it could target women 40 years old and above, i.e. the original market for Harpenne. This would further help the brand to stand out from its competitors by emphasizing its British history, in line with other fashion brands’ emphasis on their country associations with the manufacturing location, e.g. Made in Spain for ZARA and Boohoo.

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Tuesday, July 2, 2024

Iris Publishers-Open access Journal of Neurology & Neuroscience | Attention Deficit Hyperactivity Disorder (ADHD) - Symptoms Diagnosis & Treatment Incorporating Historical Perspectives

 


Authored by Caroline Goldsmith*,

Historical Implications

The modern description of attention deficit hyperactivity disorder (ADHD) was updated from early beginnings of symptom descriptions as far back as 1798, when Dr Alexander Crichton (1798) a Scottish physician, described an inattentive syndrome. Whereby the person was unable to focus on objects with a necessary degree of constancy [5]. A condition he observed which often improved with age as the person matured [1]. As a pioneer describing mental conditions with physical or medical causes, he broke away from superstitious traditions of earlier less informed times [1].

As the observation of the condition evolved it is insightful that Crichton had an inkling of the contemporary requisites seen today in the American psychiatric association fifth edition of the diagnostics and statics manual – DSM-5 (APA, 2013), of the condition being present before age seven. Crichton’s version described the presentation as ‘born with the person’ [1].

Although it has to be pointed out that Crichton made no connection to impulsivity or hyperactivity which would come to be associated with the condition in later descriptions, as understanding of presenting symptoms evolved [4]. Hyperactivity came into focus with a German psychiatrist and mental hospital reformer Dr. Heinrich Hoffman (1851), forging ahead with new ideas on mental illness away from the criminal or possession by demon ideas [6]. A particular publication was a children’s book for his son, later hailed a groundbreaking work, ‘Struwwelpeter’ translated as Troubled Peter [7], contained a story about a character called ‘Fidgety Phil’ [6] who was often jumping around when he should have been eating his dinner. Other characters in the book described behaviours that have been attributed to early descriptions of hyperactive, impulsive, and inattentive behaviours [6]. The book would go on to be widely published and translated with over 400 later editions [6].

British paediatrician Sir George Frederic Still (1902) [8] from the early nineteen hundred, often referred to as the father of British paediatrics [9], was a significant contributor to ADHD pathology being classified [8]. Still purported there was a deficit in some children of moral control that lacked three components; cognitive relation to environment, moral consciousness, and volition [8]. Still described impulsivity as an abnormal degree of passionateness [8]. An excellent description of passion not in any sense of lust or with sexual connotations, but the inability to wait to do anything.

His moral associations came from observations of children who had another symptom whereby they seemed to delight in tormenting other children [8]. It would be three decades later when Kramer [10] described a hyperkinetic syndrome [10] akin to the hyperactive component we see today with the condition. Researchers described aimless activity seen in children with a high motor engagement that seemed to be without purpose [10].

By the 1940’s connections to behaviours seen after a brain encephalitis epidemic were being made [11]. “This hyperkinesis leads the child to contact the environment continually, by touching, taking and destroying” (cited by Kessler [12]). The doctors made reference to a type of post encephalitic disease that impaired cognitive function [11] similar to modern day ADHD.

The description of hyperkinetic reaction of childhood first appeared in the DSM second edition [13] and then the term attention deficit disorder (ADD) appeared in the third edition [14]. The diagnosis of ADD was later dropped, and the new classification titled attention deficit hyperactivity disorder ADHD first appeared in the fourth edition [15]. Classification was in three distinct types; hyperactive impulsive, inattentive (formerly ADD) and combined type [15]. With the stipulation, the condition was lifelong and changing rather than resolving in adolescence as stated in previous DSM versions [14]. The current DSM 5th edition published in 2013 has retained the 1987 typology however classifies the subgroups as presentations rather than types [2].

Although the historical descriptions came in fragmented pieces a clearer picture was beginning to emerge throughout the 1950- 80’s when Dr Leon Eisenberg (2007) was working in the field of Autism research and child psychiatry [3]. He would later go on to be widely quoted out of context saying that ADHD was a fictitious disease [16], during a radio interview near his death.

Actually the utterance was in reference to how the condition was often medicated without much evidence for a biological presentation of ADHD. Evidence he stated was weak when the symptoms may be psychosocial in nature [16].

Regardless of Eisenburg’s later opinions the condition has behavioural, social, cognitive, environmental, and biological factors in a pathology that can sometimes be detected in neuro scans and imaging [3]

Dr Eisenberg was very much of the opinion that psychiatric conditions were as much social as they were biological and saw the two as inextricable intertwined [17].

Historically, disturbed or hyperactive children were seen as having bad behaviour, possession, or criminal tendencies versus the scientific approach of pathologizing children’s maladaptive behaviour as diagnosable conditions [4].

Eisenberg differentiated such notions by applying a rigorous scientific approach to his relentless pursuit of robust classification and treatment of childhood psychiatric conditions, including Autism and ADHD [17].

Such ideas would have taken time to adjust in the world as children became more thought of as human beings in their own right, as social sciences evolved [18]. Furthering the cause of children’s rights to be considered, which was greatly aided by pioneers such as Eisenberg [17].

The condition of ADHD has a very real bio/psycho/social presentation, however, children who suffered from it were more likely to be stigmatized as naughty and unruly in days gone by [3], or the product of inexperienced or liberal parenting ideas where the children lacked discipline [19].

Symptoms of ADHD

The condition of attention deficit hyperactivity disorder (ADHD) is characterised by physical, behavioural, and cognitive symptoms that are grouped into distinct presentations [4].

Hyperactivity

Children are often constantly moving, climbing, rocking the chair, tapping, poking, annoying other children and fidgeting [20]. They may also have difficulty sleeping and switching off at night [21].

Adults and children tend to be unable to concentrate unless they are on the go. Pacing around when talking on the phone for example, or unable to sit still [22].

They may have several windows open on the computer in order to get one thing done or be reading a book while watching TV. A constant compulsive need to be active and busy or moving to concentrate [22].

Impulsivity

Sufferers tend to have a tendency to act on impulse rather than giving careful thought to actions, which has been recently linked to faulty limbic signalling [23], a prevalent symptom in children which seems to improve with age. Also, the lack or reduced sense of danger seems to drive behaviours associated with risk taking [23]. Adverse consequences do not act as a protective factor as it would do in a more usual presentation of childhood reinforcing developmental experiences [24]. An absence of the usual feedback to instil a deterrent, possibly as some affected children seem to lack the signalling of a pain response and or have a high pain threshold [24]. This then affects reward processing on a neuropsychological level [25]. However this is not a disorderspecific consideration, as it can also be seen in Autistic individuals. A condition with high comorbidity with ADHD [25].

Research into this area, recently discovered therapeutic targets whereby the lack of pain response can be treated by medication [26]. This research is a great hope for affected children not just in ADHD but with Autism also, which is often seen as a comorbid presentation [27].

In Children they may be chatterboxes and engage in class disruption [28]. They can be quick to anger and aggressive or over eager, cannot take or wait their turn in games and may be bossy and dominant [29].

In Adults they are often fast talkers, with impulsivity manifesting as bad decision making. With impulsive speech and actions leading to unemployment, financial difficulties, and an unsuccessful personal life [30]. Actions which are often regretted later when the prefrontal cortex (higher decision making) engages [31]. When people act without thinking, this is because the impulse has dominated the action without sending the signal for rational decision making to complete [31]. Children make careless academic mistakes due to impulsivity and rushing things [4].

Inattention

flitting from task to task, low concentration and focus with difficulty staying on track [4]. May have to make constant lists to avoid forgetting things. Jumping to quick conclusions due to not giving due attention and considering all the facts/implications [31]. Children zone out and daydream a lot in class, while adults switch off their focus and stare into space, losing vast periods of time [23].

Cognitive symptoms

centre around executive function deficits in planning, cognitive flexibility, inhibition, abstract-reasoning, and working memory [32]. Short-term memory (STM) deficits were found to improve with physical activity, denoting memory function and motor cortex connections [33]. There is also a lack of organisational skills and continually losing things [4].

ADHD in adults is linked to procrastinators, distracted with everything except what they should be doing [34]. However, procrastination was found to correlate only with inattention, not other ADHD symptoms [34]. With afflicted individuals requiring the impending doom of failure in order to meet a deadline, While they were often creative thinkers, they tended to have low selfimage and poorer academic performance [35] than non-affected peers.

Diagnostic Criteria, Assessment and Classification

Historical presentations have evolved from diagnosis through clinical observation by a psychiatrist or medical doctor [36], to use of psychometric assessment instruments developed specifically for diagnosis and also allowed for psychologists to use [4]. As the symptoms associated with the condition evolved, so did the questions to identify them, in order to classify and identify specific presentations [18].

A good workup includes comprehensive background and developmental history, cognitive testing, behavioural presentation, physical manifestations, mental health aspects of the impact of symptoms, consideration of the social implications and adaptive function and school & home report [36]. For child assessment the forms tend to have three types of report procedure to assess from; parent/caregiver perspective, the school/creche perspective and a self- report if the child is 12 years or over [20]). Modern assessment platforms such as Pearson and MHS offer online scoring and produce diagnostic and intervention reports as stand-alone reports or as comparisons between reporters [4].

Best practice robust ADHD assessment is a mixture of comprehensive background and development reporting, clinical observation, psychometric testing, and various reporter perspectives [36].

Assessment instruments

• Cognitive testing: Stanford Binnet 5th edition (SB5), Weschler intelligence Scale for Children 5th Edition (WISC 5) Weschler Intelligence Attainment Test 3rd edition (WIAT III)

• Executive function testing: Comprehensive Executive Function Inventory (CEFI) adult and child versions

• ADHD Symptoms & Screening: Conners III, Vanderbilt ADHD Rating Scales, ADHD Rating Scale-IV (ADHD-RS-IV) children. Adult ADHD Clinical Diagnostic Scale (ACDS) v1.2, Brown Attention-Deficit Disorder Symptom Assessment Scale (BADDS) for adults

• Childhood questionnaires: Social Communication Questionnaire, Child Behavior Checklist (CBCL/6-18)

• Adaptive function assessment: Vineland Adaptive Behaviour Schedule (VABS II), Adaptive Behaviour Assessment System (ABAS-III) [37].

DSM-5 and ICD-11 childhood diagnosis classification

Diagnosis is classified under the DSM 5 (APA, 2013) or ICD- 11 [38] manuals, depending on type of symptoms, which have to be present before age seven years. Stipulating traits are seen in more than one setting for at least six months, and inconsistent with developmental level, negatively impacting social / academic / occupational function [2].

Hyperactive impulsive 314.01 (f90.1): at least 6 of the 9 symptoms present for 6 months or more in more than one setting (age 17 and over 5 symptoms) [2]

Inattentive 314.0 (f 90.0): at least 6 of the 9 symptoms present for 6 months or more in more than one setting (age 17 and over 5 symptoms) [2]

Mixed Type 314.01 (f 90.2): meets the criteria for both of the above groups by a combination of at least 6 of the 9 symptoms (age 17 and over 5 symptoms) in both of the above groups present for 6 months or more in more than one setting [2]

Differential Diagnosis - DDX

Differential diagnosis considerations are particularly relevant as the update of the DSM to the fifth edition stipulated the condition of ADHD and autistic spectrum disorder (ASD) were no longer mutually exclusive (APA, 2013). Having previously been an either/ or diagnosis, as the conditions were thought to involve separate neurobiological pathology (APA, 1980). However, the updated version of the DSM having considered the evidence was at best conflicting, opted for the possibility of dual diagnosis [2]. Likely in part driven by the literature regarding twin studies arguing against precluding dual diagnosis when considering differential diagnosis and overlapping traits [25].

The overlap is often significant and may seem simultaneous at times considering observed traits of ADHD and ASD, noting both presentations have social impairments [25].

However, with ADHD presentation, the poor social success stems from over enthusiasm, constant interrupting or almost taking over the other children [39]. Coupled with a pattern of hyperactive interactions that can be overwhelming for peers [29]. Such traits as impatience which manifest as a lack of turn taking where they are not letting other children have a go at games or activities, or impulsivity often drives them to jump queues or lines [29].

Whereas with ASD, the lack of social success is driven by a marked lack of desire for social interaction, a lack of social ability to connect on a meaningful level with peers, and social communication impairments [40].

ADHD is differentiated from the ASD presentation in the social setting, as with ASD they don’t know how or are anxiety based with a lack of social skills and sensory overload in group situations.

There is too much information coming at them at once [40]. However, in the ADHD presentation the child is coming at you full force, all the time and does not give the others a chance. Over enthusiasm and under enthusiasm would appear to both make for poor social success in childhood development.

Other similar traits are obsessions (APA, 2013), whereby both conditions may on a surface level appear similar, however the drivers are very different [25]. With ASD obsessions are driven by static neural processing which manifests as a fondness for sameness and resistance to change, so they like to stick to one focus at a time [41]. On the other hand, obsessive behaviours in ADHD are thought to be driven by compulsions linked by a corresponding neural network to obsessive compulsive disorder (OCD), which both conditions share [42].

Rapid bursts of cluttered, compulsive speech is a trait seen in a particular genetic phenotype of Autism - Fragile X Syndrome [43] and can also be a feature of ADHD [28]. However, with ADHD, language delay is usually not a feature of early development and therefor helps to differentiate [4]. With genetic testing, also a possibility, and may be in order if the background history, observation and school and home presentation does not make things clear [21].

ADHD Spectrum of function

The condition of ADHD can be mild to severe and impede function and learning across a spectrum (Conners 2001). People can come for help as children or as older adults [31] who have suffered in school missing windows of opportunity for earlier intervention [32]. They have often learned to muddle their way through life sometimes going back to education, as older adults, lamenting they could have been diagnosed and helped earlier [30].

Neurobiological Basis of ADHD

ADHD has been the subject of much research focusing on neurobiological factors, which brings the discussion back to Eisenberg (2007) on how much of the condition is psychosocial in origin and how much genetic/biological [3]. However, there is no doubt a burgeoning body of research exists regarding neurobiological factors of the condition.

Motor cortex

recent research suggests children and adults have a defined pathology with implications for the motor cortex -controlling movement [42]. Teachers used to be told to help children learn to control themselves by sitting on their hands and keeping still [44]. Now the hyperactivity is thought to have implications for children being unable to access higher thought processes in the dorsolateral prefrontal cortex (DLPFC) unless the motor cortex is also engaged. In short, they need to be hoping, popping, and moving or they cannot think or concentrate [42].

Signalling gates

ADHD is one of a range of psychiatric conditions which have been the subject of research on gene encoding for voltage-gated calcium channels (CaVs), with faulty signalling providing for pharmacology targets [45].

Density of grey matter

reduced grey matter (GM) was found in female non-white subjects which could have implications for synapses and signalling in the motor cortex of those with combined type ADHD [46].

Limbic system

impulse control impairment is implicated from emotional connections in the limbic system to the anterior midcingulate cortex (aMCC) with structural abnormalities causing impairment in impulse control and cognition - a finding suggesting why children with ADHD respond impulsively to stimuli [47].

This is just a selection of key research findings to improve understanding of the neurobiology which is key to effective intervention for the condition [36].

Treatment and Interventions

Occupational therapists (OT)

This professional will often be working with the child, the parents and education team to design a sensory diet for the child which makes sure they are wound down when over excited and stimulated when undermotivated. The goal of a sensory diet is to regulate the child’s function, so they are on an even keel [48,49].

The (OT) can design a program to engage the child’s motor cortex so they can have better concentration and attention [48,49].

Neurofeedback

Aims to strengthen connections between the limbic system and the prefrontal cortex. The children are encouraged to move objects on a screen with their mind while hooked up to a monitor and headset and find it great fun. A metanalytical study recommended training for practitioners and the furthering of standard protocols [50].

Delayed gratification

At home the parents are encouraged to delay gratification research has suggested neural circuitry can be trained by delaying gratification in

children with ADHD [51]. The marshmallow test where children were promised a bigger reward if they waited is an established delayed gratification technique that has implications for better success in later life [52]. The principal has been applied in schools and homes to let children practice waiting for things – for example if they ask for parent/teacher time, screen time or a treat they are given a card with a wait time (5, 10, 15 mins or longer) they know they will get more than what they asked for if they can wait for it.

The point is to train the mind that if you wait you get more. Eventually in time and with regular training the children can wait longer and longer to get things [53].

Motor cortex engagement

In school teachers can consult with occupational therapists and psychologists to have a movement arsenal for children with ADHD. Such things as putting elastics across the base of their chair means they can be hopping and popping when they need to concentrate or with wriggle cushion on the seat, fidget spinners, activity finger cubes [54].

Understanding of the child’s need to engage their motor cortex in order to access higher thought processes is crucial [42]. Taking movement or sensory breaks is another way to support children with ADHD traits, as in the Movi-Kids intervention [54].

Social and Communication skills

children may need social programs to help them connect more effectively with peers as they seem to have a tendency to have low social success, due to their hyperactivity and impulsivity which can drive a lack of consideration for other’s needs [39].

Counselling

Including community involvement between home and school, play therapy, family therapy and CBT – have all shown to have a role in the treatment and management of ADHD [55].

Medication

A range of medications have been tried for the condition when it was discovered that brain receptors could be targets for pharmacology intervention [56]. Children diagnosed with ADHD are often referred to psychiatry for an appraisal to see if medication has a role to play [57].

Sleeping

They can be medicated to sleep and get a good rest as the melatonin receptor seems to be at odds with over production of adrenalin and cortisol which does not dissipate at night [57]

Concentration, Impulsivity, and Inattention are all pharmacology targets which have been shown to have useful and effective results for ADHD [56].

The history of medications associated with ADHD is a chequered one with arguments about children being medicated too much or too little [1].

The ritalin crisis

Methylphenidate, a stimulant produced under brands such as Ritalin and Concerta, is often the first- line drug of choice in ADHD childhood presentation [56]. Such medication, especially the brand Ritalin came under fire in the 1980’s, when children were more freely medicated [56]. Resulting in somewhat of a divide in the medical community for a nonmedicated versus medicated approach to the condition. Much research has been done suggesting that non pharmacology interventions are tried first and then a combination of pharamacology, along with other approaches can be tried for the patient [56].

Conclusion

ADHD has an evolving history from late 1700 [1]. Symptoms and traits of Inattention, impulsivity, hyperactivity and cognitive deficits in various combinations, changing throughout the lifespan, having a negative impact on social, academic and community function [3]. Diagnostic criteria according to type are set out in the DSM-5 [2] and ICD-11 [52]. The neurobiological basis of ADHD has provided pharmacology, psychosocial and academic setting interventions [27]. Medication targets sleeping, concentration, inattention, impulse control and cognitive function [56]. A good intervention regimen depends on a combined approach and with caregivers and professionals working together [56,58-60].

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