Pusher Syndrome  推進癥候群

Original Editor - Lizzie Cotton

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Introduction  簡介[edit | edit source]

First described by Patricia Davies in 1985, [1] "Pusher Syndrome" is a term used to describe the behaviour of individuals using their non-paretic limb to push themselves towards their paretic side. Left unsupported, these patients demonstrate a loss in lateral posture, falling onto their paretic side. [2]
1985 年由 Patricia Davies 首次描述，"推力症候群"用來描述個體使用非癱瘓肢體推自己到癱瘓側的行為。若無支撐，這些患者會失去側向姿勢，傾向於倒在癱瘓側。 [1]

Pusher Syndrome (also has been referred to as contraversive pushing , ipsilateral pushing or lateropulsion[3]) is a motor behavior characterized by active pushing with the stronger extremities towards the hemiparetic side with a lateral postural imbalance,[4] generally seen after stroke [5] and is often accompanied by severe inattention and hemisensory impairments. [1][6] Incidence of this disorder after stroke is inconsistent in the literature; ranging from approximately 5-10% [7] [8] to 63% [9].
推動症候群（也稱為對側推移、同側推移或側向推移 [3] ）是一種運動行為，表現為使用較強的肢體向患側推移，並伴有側向姿勢失衡， [4] 通常在中風後 [5] 出現，常伴有嚴重的注意力不集中和半側感覺障礙。 [1] [6] 中風後此種癥狀的發病率在文獻中不一致，從約 5-10% [7] [8] 到 63% [9] 。

Clinically Relevant Anatomy
臨床相關解剖學[edit | edit source]

The tilted orientation of the body verticality in people with pusher syndrome was found to be associated with the lesion of the posterior thalamus. [10]
有推動症的患者身體垂直方向的傾斜與後側丘腦的病變有關。 [10]

Thalamus is a structure of the diencephalon. It has different nuclei formed mainly by neurons of excitatory and inhibitory nature and each with a unique speciality. It is mostly composed of grey matter. The white matter parts are external medullary laminae covering the lateral surface of the thalamus and internal medullary laminae dividing the nuclei into three (anterior, medial and lateral) groups. [11]
丘腦是中腦的一部分。它由主要由興奮性和抑制性神經元形成的多個核團組成，每個核團都有獨特的功能。它主要由灰質構成。白質部分是覆蓋丘腦側面的外側髓質層和分隔核團為前側、中側和側側三組的內側髓質層。 [11]

The posterior thalamus plays a fundamental role in the control of upright body posture. [10] Some nuclei in this part of the thalamus are sensitive to vestibular stimulation. [12][13]
丘腦後側在控制直立姿勢中扮演著關鍵角色。 [10] 這部分丘腦中的某些核團對前庭刺激敏感。 [12] [13]

Pathological Process  病理過程[edit | edit source]

Despite the increase in investigation in the causes and symptoms of Pusher Syndrome, it is still a poorly understood presentation. It has been suggested that Pusher behaviour may be a result of a conflict between an impaired somesthetic perception of vertical, and intact visual system or that it may be a consequence of a high-order disruption of somatosensory information processing from the paretic hemi-body.[14] Patients with Pusher Syndrome may also have primary visual or visual perceptual problems, impaired proprioception, and motor impairments, which leave them less able to relearn posture and balance. [15]
尽管對推 Syndrome 的原因和症狀進行了更多的研究，但它仍然是一種理解不足的表現。有人認為，推行為可能是由於對垂直的感覺運動感知受损和完整的視覺系統之間的衝突，或者可能是由於對患側半身的高級感覺信息處理的干擾所致。 [14] 患有推 Syndrome 的患者也可能有主要視覺或視覺知覺問題、 proprioception 损害和運動障礙，這使他們更難重新學習姿勢和平衡。 [15]

Karnath et al demonstrated that patients with Pusher Syndrome have a misperception of their upright body posture; with patient’s reporting an “upright” posture when actually tilted 18 degrees to the ipsilesional side. With MRI scanning, the patients included in this study typically demonstrate left or right posterolateral thalamus damage post stroke. [10] However the evidence around location of infarct is conflicting with some studies also suggesting damage to the parietal area. [2] [14]
Karnath 等人表明，患有推 Syndrome 的患者對其直立身體姿勢存在誤感知；患者報告其為“直立”姿勢，實際上是向 ipsilesional 側傾斜了 18 度。通過 MRI 扫描，本研究中包括的患者通常顯示出中風後左側或右側後外側丘腦損傷。 [10] 然而，關於梗塞位置的證據存在矛盾，一些研究也建議丘腦後部或頂葉區域的損傷。 [2] [14]

Several previous studies suggested that pusher behavior was more observed in patients with right brain damage than in patients with left brain damage [16]. Abe et al also suggested that there could be increased prevalence of Pusher Syndrome with right sided hemisphere damage [17]. Paci et al in their review suggested that the range of evidence in Pusher Syndrome may be due to a multidimensional network responsible for upright postural control. [14]
几项先前的研究表明，右腦損傷的患者比左腦損傷的患者更容易出現推床行為 [16] 。Abe 等人也提出，右側半球損傷可能會增加推床症候群的發病率 [17] 。Paci 等人在其綜述中指出，推床症候群的證據範圍可能歸因於多維度網絡，負責維持直立姿勢控制。 [14]

Schematic drawing of pusher patients' perceived postural vertical (SPV) with occluded eyes (A) and while viewing their surroundings (B). The patient's SPV shows a marked ipsiversive deviation from the earth-vertical with occluded eyes.
Schematic drawing of patients with pusher syndrome's perceived postural vertical (SPV) with occluded eyes (A) and while viewing their surroundings (B). The patient's SPV shows a marked inversive deviation from the earth-vertical with occluded eyes.
患有推床症候群的患者在閉眼（A）和觀看周圍環境（B）時的感知垂直（SPV）圖形。患者在閉眼時的 SPV 顯示出顯著的倒立偏差。

Clinical Presentation  臨床表現[edit | edit source]

Kim and Seok-Hyun [16] identified the following symptoms on patients with Pusher Syndrome:
Kim 和 Seok-Hyun [16] 在患有推床症候群的患者中識別出以下症狀：

  • Flexed position of affected side limbs
    受影響側肢體的屈曲位置
  • Extended position of the unaffected side limbs
    未受影響側肢體的伸展位置
  • Severe damage to the balance ability ( loss of postural balance)
    嚴重的平衡能力損傷（站竜平衡失常）
  • Severe altered perception of the body's orientation in relation to gravity
    身體對重力的定向有嚴重的錯覺
  • Resistance to any attempts to rectification
    任何試圖改正的抵抗
  • Normal visual and vestibular system function
    正常的視覺和前庭系統功能
  • Spatial neglect and anosognosia with right brain injury
    空間忽略和無自知之明，右腦受傷
  • Spatial aphasia with left brain injury
    空間失語，左腦受傷

Diagnostic Procedures  診斷程序[edit | edit source]

Karnath and Broetz [18] identify three diagnostic factors of Pusher Syndrome, as shown below:
Karnath 和 Broetz [18] 識別出推 Syndrome 的三個診斷因子，如下所示：

  1. Spontaneous Body Posture (severe/moderate and mild)
    自发體位（嚴重/中度和輕度）
    The patient’s initial posture shown immediately after a positional change (ideally supine to sit/ sit to stand) must be assessed for contralateral tilting. This can be seen with or without falling to the side contralateral to the brain lesion. It is felt that patient’s must demonstrate this postural abnormality regularly to be classified as suffering with Pusher Syndrome.
    患者的初始姿勢在位置改變後立即顯示（理想情況下為平躺轉為坐姿或坐姿轉為站立），必須評估是否有對側傾斜。這可能在側傾向對側腦損傷的對側側倒時或無側傾時均可見。認為患者必須定期顯示這種姿勢異常才能被診斷為患有推 Syndrome。

  2. Abduction and Extension of the Nonparetic Extremities
    非癱瘓側肢體的提舉及伸展
    Patients demonstrate abnormal positioning of the side ipsilateral to the brain lesion. Typically the hand will be abducted away from the body, the elbow held in extension and the hand searching for contact with a surface on which to push oneself to the perceived upright position. The lower limb may be abducted, with the knee and hip held in extension (as with the upper limb).
    患者顯示腦損傷對側的側位異常定位。通常手會向外展離身體，肘部保持伸直，手會尋找表面以推自己到感知的直立位置。下肢可能也會向外展，膝蓋和髋關節保持伸直（與上肢相同）。

  3. Resistance to Passive Correction of Tilted Posture
    抵抗/passive 校正傾斜姿勢的抵抗力/correction
    Patients will typically actively resist against therapist’s manual interventions to correct their body posture. The patient’s extended upper and lower limbs will be used to push their weight towards their paretic side.
    患者通常會主動抵抗治療師的手動干預，以糾正他們的姿勢。患者的伸展上肢和下肢會被用來將他們的重量推向癱瘓側。

Subsequently, the Standardized Scale for Contraversive Pushing (SCP), has been formulated on these 3 deficits. The SCP is a useful tool for clinicians to classify Pusher Syndrome, and is quick and easy to apply in both an acute and rehabilitation setting [19].
Subsequently, the Standardized Scale for Contraversive Pushing (SCP)，已在這三項缺點的基础上制定出來。SCP 是一種對推 Syndrome 進行分類的有用工具，並且在急診和康復設施中都很容易應用 [19] 。

Outcome Measures  結局的測量指标[edit | edit source]

Burke Lateropulsion Scale
伯克側推量表[edit | edit source]

  • This scale assesses the patient’s resistance to:
    本量表評估患者的抵抗能力：
    • Passive supine rolling  被動仰臥翻轉
    • To passive postural correction when sitting and standing
      由坐姿轉為站立姿勢的被動姿勢校正
    • To assistance during transferring and walking.
      轉移和行走時的協助。
  • The score for each component s rated on a scale from 0 to 3 (0 to 4 for standing) and the score is based on the severity of resistance or the tilt angle when the patient begins to resist the passive movement. The score for diagnosis of Pusher behaviour is ≥2 points . [20]
    每個組成部分的分數根據 0 至 3 （站立時為 0 至 4）的比例尺評定，分數基於患者開始抵抗主動運動時的抵抗程度或傾斜角度。診斷推行為的分數為≥2 分。 [20]

Scale for Contraversive Pushing
對側推舉量表[edit | edit source]

  • This is made up of 3 components
    這由 3 個組成部分組成
    • The symmetry of spontaneous body posture (rated with 0, 0.25, 0.75, or 1 point)
      自发體位的對稱性（以 0、0.25、0.75 或 1 分評分）
    • The use of non-paretic extremities (0, 0.5, or 1 point)
      非癱瘓肢體的使用（0、0.5 或 1 分）
    • The resistance to passive correction of the tilted posture (0 or 1 point).
      調整傾斜姿勢的抵抗程度（0 或 1 分）。
  • For a diagnosis of Pusher Syndrome all 3 components need to be present. [20]
    要診斷為推移癥候群，所有 3 個組成部分都需要存在。 [20]

Bergmann et al suggested that the Burke Lateropulsion Scale is more sensitive to small changes in presentation and is more responsive in classifying Pusher behaviour than the Scale for Contraversive Pushing. In addition it was suggested that the Burke Lateropulsion Scale is especially useful to detect mild or resolving pusher behaviour in standing and walking.[20]
Bergmann 等人建議，Burke 側推量表對於檢測呈現上的微小變化更靈敏，並且在分類推移行為方面比對角反推量表更具反應性。此外，建議 Burke 側推量表特別適合用於站立和行走時檢測輕微或正在恢復中的推移行為。 [20]

Management / Interventions
管理 / 干預措施[edit | edit source]

Karnath and Broetz [18] suggested that the first goal of initial rehabilitation is to provide visual feedback of the patient’s altered body posture. By providing patients with visual information in relation to their environment they are able to feel they are in an erect posture when they see that they are tilted. While in different postural sets patients should be asked whether they see if they are upright and given visual references/cues to help them orientate themselves to upright and given them feedback about their body orientation. For example by using ground-vertical structures- ie a therapist’s arm held upright to demonstrate true upright orientation, a line on a wall or a door frame. Although patients with Pusher Syndrome may initially need prompting with the use of visual feedback it is hoped that, with regular therapy, patients are able to apply training procedures independently and utilise their environment for gaining visual feedback from vertical structures [21].
卡恩和布雷茨 [18] 設計初始康復的第一個目標是提供患者改變後姿勢的視覺反饋。通過提供患者與其環境相關的視覺信息，當他們看到自己傾斜時，他們能夠感到自己是直立的姿勢。在不同的姿勢設定中，應詢問患者是否看到自己是直立的，並提供視覺參考/提示，幫助他們對準直立姿勢並反饋他們的身體姿態。例如，使用地面垂直結構，即治療師舉起的垂直手臂以展示真正的直立姿態，牆上的線或門框。雖然患有推擠症狀的患者最初可能需要使用視覺反饋的提示，但希望通過定期治療，患者能夠獨立應用訓練程序並利用環境從垂直結構獲得視覺反饋 [21] 。

Kim and Seok-Hyun suggested the stimulation of the trunk flexor with the appropriate lower muscle tone as well as maintaining the posture with the trunk moving in the direction of the given goal [16].
金和 Seok-Hyun 建議通過適當的下肢肌張力刺激脊柱屈曲，並保持姿勢，使脊柱朝給定目標的方向移動 [16] 。

Karnath and Broetz suggested from their clinical experience that the following sequence of treatment may be effective in treatment of Pusher Syndrome:
卡納特和布雷茨根據他們的臨床經驗建議，以下治療順序可能對推物癥的治療有效：

  • Enable the patient to visually explore their surroundings and the body's relationship to their environment and see whether he or she is oriented upright. Reference points can be used such as the therapist's arm or many vertical structures, such as door frames, windows or pillars.
    使患者能夠視覺探索其周圍環境及其身體與環境的關係，並檢查他或她是否保持直立。可以使用參考點，如治療師的手臂或許多垂直結構，如門框、窗戶或柱子。
  • Practicing movements necessary to reach a vertical body position.
    践行達到直立身體位置所需的動作。
  • Performing functional activities whilst maintaining a vertical body position [18].
    保持直立身體位置的同時進行功能活動 [18] 。

More recent treatments suggest to: [16]
更新的治療建議： [16]

  • Enable the patient to realize the disturbed perception of upright body position.
    使患者能夠意識到其身體直立位置的錯覺。
  • Learn the movements that are necessary to reach a vertical body position.
    學習達到垂直身體位置所需的動作。


Other recent treatment options that found to be useful are: interactive visual feedback training, mirror visual feedback training [22], lateral stepping with body weight–supported treadmill training [23] robot-assisted gait training [24], standing frame [25].
其他被發現有用的最近治療選項包括：互動視覺反饋訓練，鏡像視覺反饋訓練 [22] ，側向踏步輔助踏車訓練 [23] 、機器人輔助步態訓練 [24] 、站立架 [25] 。

Abe et al suggested that when considering length of rehabilitation stay that laterality and prognosis of Pusher Syndrome should be considered at the time of goal setting for rehabilitation [17].
阿貝等人建議，在設置康復目標時，應考慮推综合征的側向性和預後情況 [17] 。

[26]

Prognosis  預後[edit | edit source]

There are conflicting opinions in the literature with regards to the persistence of Pusher Syndrome in the longer term and its impact on functional outcome. Some authors report that the presence of Pusher Syndrome is rarely seen 6 months post stroke and is shown to have no negative impact upon patients’ ultimate functional outcome, although it has been shown to slow rehabilitation by up to 3 weeks [18]. However, a case study by Santos-Pontelli et al [2] reported the lingering presence of Pusher Syndrome in 3 patients up to two years post-stroke, with profound negative impacts upon their functional abilities.
文獻中對推综合征在長期中是否存在及其對功能結果的影響存在爭議。一些作者報告稱，中風後 6 個月內很少見到推综合征，且顯示出它對患者最終的功能結果沒有負面影響，儘管它已被證明會延長康復時間最多 3 周 [18] 。然而，桑托斯-蓬蒂等人 [2] 的病例研究報告稱，在中風後兩年內，仍有 3 名患者存在推综合征，對他們的功能能力造成了深刻的負面影響。

In a study by Babyar et al they reviewed whether the number of impairments patients with Pusher Syndrome had, was a determinant on the level of recovery achieved [15] From their findings they proposed that 90.5% of patients studied with only a motor presentation were able to 'recover' (scoring 0 or 1 in the Burke Lateropulsion Scale) from Pusher Syndrome within 27 days. Those patients with with 2 deficits achieved the target in about 59% of cases.For patients with motor, proprioceptive, and visual–spatial impairments or hemianopia however, only 37% of patients were able to achieve a score of 0 or 1 on the Burke Lateropulsion Scale prior to discharge.
在 Babyar 等人的一項研究中，他們審視了患 Pusher 症狀的患者所出現的障礙數量是否能決定其恢復程度。根據他們的研究結果，90.5%的患者在只有運動障礙的情況下，能在 27 天內從 Pusher 症狀中恢復（在 Burke 側推量表上得分 0 或 1）。那些有兩種缺陷的患者，約有 59%的案例能夠達到目標。然而，對於那些有運動、本體感、視覺-空間障礙或同向偏盲的患者，只有 37%的患者能在出院前在 Burke 側推量表上達到得分 0 或 1。

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Differential Diagnosis  差別診斷[edit | edit source]

A clinical picture similar to pusher syndrome may occur in patients with hemiparesis because of the loss of balance. In this sense, the term contraversive pushing is distinctive as it emphasizes the pushing of the non-hemiparetic extremities towards the contralateral side of the brain lesion. In addition, the hemiparetic patient without pushing syndrome realizes that he/she has lost his balance and tries to hold onto something to support himself/herself with his non-paretic hand, so presents pulling rather than pushing. [18] But the patient with pushing syndrome resists any attempt to correct their tilted position. [27]
患者因失去平衡而出現類似推擠症候群的臨床表現，這在半身痙攣的患者中可能會發生。因此，「對側推擠」這個術語是獨特的，因為它強調的是非半身痙攣極端向對側腦損傷部位推擠。此外，沒有推擠症候群的半身痙攣患者會意識到自己失去平衡，並會用非痙攣側的手抓住某物以支持自己，因此表現為拉扯而非推擠。 [18] 但是，有推擠症候群的患者會抗拒任何嘗試糾正其傾斜姿勢的行為。 [27]

Resources  資源[edit | edit source]

The "Pusher" syndrome, assessment and treatment: Part 1 [28]
推擠症候群：評估與治療：第一部分 [28]

The “Pusher “syndrome, assessment and treatment: Part 2 [29]
推擠症候群：評估與治療：第二部分 [29]

Related articles  相關文章
Thalamus - Physiopedia  背顱核 - 物理治療百科 Thalamus Structure The thalamus is located centrally in the brain, just above the brainstem. The thalamus is located medial to the cerebral hemispheres and consists of two oval-shaped masses connected by the intermediate mass. Each mass consists of several groups of nuclei that serve different functions. Motor and sensory pathways (except olfaction) pass through this central structure. The thalamus can be divided into approximately 60 regions known as thalamic nuclei. Each nucleus has unique pathways as inputs and various projections as outputs, most of which send information to the cerebral cortex.[1] Hypothalamus[edit | edit source] Located inferior to the thalamus Two rounded eminences protrude from the back, called mammillary bodies Anteriorly, the hypothalamus is connected to the pituitary gland by a long stalk called the infundibulum, also known as the pituitary stalk The hypothalamus plays a major role in maintaining homeostasis via the autonomic nervous system, the neuroendocrine system, and the limbic system. It regulates emotions, hormone production from the pituitary gland, and bodily functions such as appetite, body temperature, reproduction, and circadian rhythms. Epithalamus[edit | edit source] Located behind the thalamus Includes the pineal gland, which secretes the hormone melatonin in response to darkness, regulating our circadian rhythms and sleep-wake cycles Subthalamus[edit | edit source] Located beneath the thalamus Includes the subthalamic nucleus, which is functionally considered part of the basal ganglia Function of the Thalamus[edit | edit source] The thalamus functions as a relay station between the brain and the body, filtering through various types of sensory and motor information. Note the central location of the thalamus in relation to other subcortical structures and the cerebral cortex. The thalamus has many connections with the cerebral cortex,[1] which are known as thalamacortical loops It transmits nearly all sensory information to the cortex, including vision, taste, touch and balance, but excludes olfactory information It conducts motor signals from the cerebral cortex to the spinal cord and ultimately to the peripheral nervous system The thalamus also modulates arousal mechanisms, maintains alertness, and directs attention to sensory events[2] The thalamus has connections with a number of structures of the limbic system, including the hippocampus, mammillary bodies, and fornix, so it has a role in learning and episodic memory[1] The thalamus can be divided into five major functional components.[1] Reticular and intralaminar nuclei: involved in arousal and pain regulation Sensory nuclei: regulate sensory domains, apart from olfaction Effector nuclei: govern motor and language functions Associative nuclei: involved in cognitive functions Limbic nuclei: manage mood and motivation These specific nuclei help to scan the cerebral cortex and determine active brain regions, relaying this information to the rest of the thalamus.[2] Thalamus and Injury[edit | edit source] The thalamus is involved in many critical functions and injury to the thalamus can cause a range of issues, including: sensory issues (e.g. pain, paraesthesia, numbness, hypersensitivity) vision impairment and light sensitivity motor impairment tremor issues with attention memory impairment sleep difficulties proprioception impairment The following presentations are unique to thalamic injury: thalamic pain syndrome: an excruciating sensation of pain that does not respond to narcotics. Once called Dejerine-Roussy Syndrome, this condition is commonly associated with infarction of the ventroposterolateral thalamus.[3] [4] Pusher syndrome (also referred to as "persons who push"): a lesion to the posterior thalamus interrupts the connection to the vestibular nuclei, leading to lateropulsion in the direction of the affected side.[5] vegetative state and coma: a lesion to the non-specific (intralaminar and reticular) nuclei.[6] Coma may occur due to the role of the thalamus in sleep and arousal. Additional Resources[edit | edit source] For more information on treatment options, please read the following articles: Traumatic Brain Injury Traumatic Brain Injury Clinical Guidelines Physiotherapy Management of Traumatic Brain Injury Physical Activity Guidelines for Traumatic Brain Injury Stroke: The Role of Physical Activity Stroke: Clinical Guidelines Post-Stroke Pain Mirror Therapy Management of pushing tendencies Desensitisation for thalamic pain
丘腦結構 丘腦位於腦部中央，位於腦幹之上。丘腦位於腦半球內側，由兩個橢圓形的團塊組成，這兩個團塊由中間團塊連接。每個團塊由幾個負責不同功能的核團組成。運動和感覺通路（除嗅覺外）均通過此中央結構。丘腦可以分為約 60 個區域，稱為丘腦核。每個核團有獨特的輸入途徑和多種投射，大多數會將信息傳送到大腦皮層。[1] 下丘腦[編輯 | 編輯源代码] 位於丘腦之下 后面有兩個隆起，稱為乳頭體 前方，下丘腦通過一長柄稱為垂體柄（也稱為垂體柄）與垂體腺連接 下丘腦通過自主神經系統、神經內分泌系統和邊緣系統維持內環境穩態。它調節情緒、垂體腺的激素分泌以及食欲、體溫、生殖和生物節律等身體功能。 Epithalamus[編輯 | 編輯源碼] 位於丘腦後方 包含松果體，松果體在黑暗中分泌褪黑激素，調節我們的生理時鐘和睡眠-清醒週期 Subthalamus[編輯 | 編輯源碼] 位於丘腦下方 包含次丘核，功能上屬於基底核的一部分 脑中的丘腦功能[編輯 | 編輯源碼] 丘腦作為大腦和身體之間的中繼站，過濾各種感覺和運動信息 注意丘腦在其他次皮質結構和大腦皮層之間的中心位置。 丘腦與大腦皮層有許多連接，這些連接稱為丘腦皮質回路。它幾乎傳導所有感覺信息到皮質，包括視覺、味覺、觸覺和平衡感，但不包括嗅覺信息。它傳導大腦皮質的運動信號到脊髓，最終到周圍神經系統。丘腦還調節觉醒機制，保持警覺性，並將注意力引向感覺事件。丘腦與許多边缘系统結構有連接，包括海馬體、乳頭體和 fornix，因此它在學習和情景記憶中起著作用。丘腦可以分為五個主要的功能部分。網狀核和內層核：參與觉醒和疼痛調節。感覺核：調節感覺領域，除嗅覺外。效應核：管理運動和語言功能。聯結核：參與認知功能。边缘核：管理情緒和動機。這些特定的核幫助掃描大腦皮層，確定活躍的大腦區域，並將此信息傳遞給丘腦的其他部分。丘腦和損傷[編輯 | 編輯源] 丘腦參與許多關鍵功能，丘腦損傷可能會引起一系列問題，包括：感覺問題（例如：疼痛、異感症、麻木、超敏反應）視覺障礙和對光的敏感度運動障礙顫抖注意力問題記憶障礙睡眠困難本體感障礙丘腦損傷特有的症狀包括：丘腦痛綜合徵：一種對止痛藥無效的劇烈疼痛感。 以往稱為德傑雷-羅斯綜合徵，此症狀常與背外側丘腦梗塞有關[3] [4]。推 Syndrome（也稱為「推者」）：後丘腦的損傷中斷了與前庭核的連接，導致向受損側的偏推。[5] 植物人狀態和昏迷：非特異性（內層和網狀）核團的損傷。[6] 昏迷可能由於丘腦在睡眠和清醒中的作用而發生。更多資源[編輯 | 編輯源] 請閱讀以下文章以獲取治療選項的更多信息：腦外傷腦外傷臨床指南腦外傷物理治療管理腦外傷運動指南腦中風運動活動的作用腦中風臨床指南中風後疼痛鏡像療法推動傾向的管理對於丘腦疼痛的去敏感化 Ageing Effects on Motor Control - Physiopedia
年齡對運動控制的影響 - 理療百科 Summary Motor control is the individual's abiliy to direct and regulate movement[1]. Neural control of movement involves coordination between large numbers of different structures within the nervous system. Motor control impairments in older adults are caused by medical conditions which primarily affect this population (i.e. not as a result of the normal ageing process), such as Parkinson's and stroke. They can be caused by impairments of both the motor and sensory systems. Motor system: Abnormal tone Paresis Ataxia Hypokineisa Fractionated movement deficits Sensory system: Perceptual deficits Somatosensory deficits Motor System Impairments[edit | edit source] Abnormal tone[edit | edit source] Muscle tone = the resistance of muscle to passive elongation or stretch[2]. Hypertonicity[edit | edit source] Hypertonicity, increased muscle tone, occurs as a result of loss of supraspinal inhibition to the spinal cord and is usually caused by damage to either the corticospinal tract or to the parietal lobe (from where 40% of the fibres of the corticospinal tract originate[3]).  Spasticity = a velocity-dependent increase in tonic stretch reflexes (muscle tone)[4], common in Stroke. Rigidity =  non-velocity-dependent increase in resistance to passive movement in any direction[5], common in later stages of Parkinson's. Hypotonicity[edit | edit source] Hypotonicity, ie. reduced muscle tone, is defined as a decreased resistance to passive movement, and reduced or absent stretch reflex response. It occurs as a result of decreased or absent neural drive to the muscles[6], and is seen in a number of conditions affecting older adult people including degenerative neuromuscular diseases and the early stages of stroke, in addition to peripheral nerve damage. Paresis[edit | edit source] This is the single most common motor impairment; it is defined as the reduced ability to voluntarily activate the spinal motorneurons[7]. It occurs primarily as a result of damage to the corticospinal system (ie. the motor cortical areas, the corticospinal tract and the spinal cord. Paresis occurs in a wide range of neurological disorders common in the older population, including stroke, multiple sclerosis and peripheral neuropathy. Ataxia[edit | edit source] This is a lack of coordination between movements and/or body parts, e,g, during gait, and occurs as a result of damage to the cerebellar inputs, outputs, and/or cerebellar structures. Tone is usually reduced and reflexes may be pendular[8] e.g. lower limb oscillates when patellar tendon reflex is tested[9]. Conditions which can cause ataxia include stroke, multiple sclerosis and spinocerebellar atrophies. Hypokinesia[edit | edit source] This is primarily associated with Parkinson's and sometimes with dementia, and is characterised by slow movement (bradykinesia) or absence of movement (akinesia) and is usually caused by damage to the basal ganglia. Typically, people with hypokinesia struggle with the onset of movement, and can freeze during movement[10]. Fractionated  movement deficits[edit | edit source]  This is defined as reduced ablity to isolate or fractionate movement. Many different central nervous system pathologies  which affect the corticospinal system and cause reduced ability to selectivvely activate muscles can result in  fractionate movement deficits, including stroke and multiple sclerosis. Sensory Impairments[edit | edit source] Conditions which cause motor impairments frequently also cause sensory impairments. Somatosensory loss: this can have either a central or peripheral nervous system origin. The main effect on motor control is a reduction in the accuracy of the ongoing monitoring of movement. In many people with somatosensory loss, there is increased reliance on the visual system to plan and monitor movements. Perceptual deficits: eg. "pusher syndrome" where a person who has had a stroke or brain injury pushes with the unaffected limbs toward the affected side[11].
總論運動控制是个體指揮和調節運動的能力[1]。運動的神經控制涉及神經系統內不同結構之間的協調。老年人的運動控制障礙是由主要影響該群體的醫學條件所導致（即不是由於正常的老化過程），例如帕金森病和中風。這些障礙可以由運動和感覺系統的障礙引起。運動系統：異常張力、偏癱、共濟失调、低動能、分段運動缺陷。感覺系統：知覺障礙、體感障礙。運動系統障礙[編輯 | 編輯源代码]異常張力[編輯 | 編輯源代码]肌肉張力＝肌肉對被動拉伸或伸展的抵抗力[2]。高張力[編輯 | 編輯源代码]高張力，肌肉張力增加，是由於脊髓的上行抑制喪失所導致，通常是由大腦皮層脊髓束或頂葉（大腦皮層脊髓束 40%的纖維起源於此）的損傷所引起。僵硬＝速度依賴性的伸展反射增強（肌肉張力）[4]，常見於中風。 僵硬 = 任何方向上的非速度依賴性增加的主動-passive 抗阻[5]，常見於帕金森病的後期階段。低張力[編輯 | 編輯源]低張力，即減低的肌肉張力，定義為減低的主動-passive 抗阻，以及減低或消失的伸展反射反應。它是由神經驅動力減低或消失所導致[6]，並見於多種影響老年人的疾病，包括神經肌肉退化性疾病和中風早期，以及周圍神經損傷。偏癱[編輯源]這是單一最常見的運動障礙；定義為減低的自主激活脊髓運動神經元的能力[7]。它主要由於大腦皮層脊髓系統的損傷（即大腦運動區域、大腦皮層脊髓束和脊髓）而發生。偏癱見於老年人群中多種神經系統疾病，包括中風、多發性硬化和周圍神經病。 ataxia[編輯 | 編輯源碼]這是運動和/或身體部位之間協調能力的缺乏，例如步態，並由於小腦輸入、輸出和/或小腦結構的損傷而發生。通常肌肉張力會降低，反射可能呈擺盪狀[8]，例如當測試髌腱反射時下肢會搖晃[9]。可導致 ataxia 的條件包括中風、多發性硬化和脊髓小腦萎縮。運動減少[編輯 | 編輯源碼]這主要與帕金森病有關，並且在某些情況下與失智症有關，其特徵是運動緩慢（運動減緩）或無運動（運動障礙），通常是基底核受損所致。通常，運動減少的人在運動開始時會遇到困難，並且在運動中可能會凍結[10]。分段運動缺陷[編輯 | 編輯源碼]這被定義為分離或分段運動能力降低。影響運動皮質脊髓束系統並導致選擇性激活肌肉能力降低的多種中樞神經系統病變都可能導致分段運動缺陷，包括中風和多發性硬化。 感官障礙[編輯 | 編輯源] 造成運動障礙的條件通常也會造成感官障礙。本體感缺失：這可以源自中樞神經系統或周邊神經系統。對運動控制的主要影響是對運動進行持續監控的精確度降低。許多本體感缺失的人會更加依賴視覺系統來規劃和監控運動。知覺缺損：例如，中風或腦損傷後的「推者症候群」，患者會用未受影響的肢體向受影響的一側推[11]。 Modified version of PASS - Physiopedia
修改後的 PASS - 理療百科 Search Search Search Toggle navigation pPhysiopedia pPhysiopedia About News Contribute Courses Resources Shop Contact Login pPhysiopedia About News Contribute Courses Resources Shop Contact p + Contents Editors Categories Cite Contents loading... Editors loading... Categories loading... When refering to evidence in academic writing, you should always try to reference the primary (original) source. That is usually the journal article where the information was first stated. In most cases Physiopedia articles are a secondary source and so should not be used as references. Physiopedia articles are best used to find the original sources of information (see the references list at the bottom of the article). If you believe that this Physiopedia article is the primary source for the information you are refering to, you can use the button below to access a related citation statement. Cite article Modified version of PASS Jump to:navigation, search  MODIEFIED POSTURAL ASSESMENT SCALE FOR STROKE (PASS)[edit | edit source] Only one attempt per item is allowed. Ensure that the patient manages the criteria for the scores below, as well as the criterion for the registered score. A stopwatch is used in items 4 and 7-9 where the patient should maintain a position within a specific time. Item 4 should be performed with the patient´s feet supported on the floor. In items 1-3, 5-6 and 10-12, the patient´s postural balance/control should be scored according to different degrees of support. 1. Supine to affected side lateral  Cannot perform the activity - 0 Can perform the activity with support from 2 persons-1 Can perform the activity with support from 1 person   -2 Can perform the activity without any help - 3 2. Supine to non affected side lateral  Cannot perform the activity-0 Can perform the activity with support from 2 persons -1 Can perform the activity with support from 1 person-2 Can perform the activity without any help  -3 3. Supine to sitting up on edge of bed Cannot perform the activity -0  Can perform the activity with support from 2 persons-1 Can perform the activity with support from 1 person -2 Can perform the activity without any help-3 4. Sitting without support Cannot sit-0  Can sit with slight support, for example by 1 hand-1 Can sit for more than 10 seconds without support- 2  Can sit for 5 minutes without support-3 5. Sitting to standing up  Cannot perform the activity -0 Can perform the activity with support from 2 persons -1  Can perform the activity with support from 1 person -2 Can perform the activity without any help -3 6. Standing with support  Cannot stand, even with support - 0  Can stand with strong support from 2 persons  -1 Can stand with moderate support from 1 person - 2  Can stand with support of only 1 hand-3 7. Standing without support  Cannot stand without support -0   Can stand without support for 10 seconds or leans heavily on 1 leg -1  Can stand without support for more than 1 minute or stands slightly asymmetrically -2  Can stand without support for more than 1 minute and at the same time draw hand/s from forehand to neck (like drawing finger throw the hair) altered with arm/s hanging parallel with the trunk to avoid tiredness-3 8. Standing on non paretic leg  Cannot stand on the non paretic leg  -0  Can stand on the non paretic leg for a few seconds  -1  Can stand on the non paretic leg for more than 5 seconds - 2  Can stand on the non paretic leg for more than 10 seconds  -3 9. Standing on paretic leg Cannot stand on the non paretic leg -0  Can stand on the non paretic leg for a few seconds -1  Can stand on the non paretic leg for more than 5 seconds -2  Can stand on the non paretic leg for more than 10 seconds-3 10. Standing, picking up a shoe from the floor  Cannot perform the activity - 0  Can perform the activity with support from 2 persons -1  Can perform the activity with support from 1 person - 2  Can perform the activity without any help -3  1. Sitting down from standing up  Cannot perform the activity -0  Can perform the activity with support from 2 persons -1  Can perform the activity with support from 1 person -2  Can perform the activity without any help -3 12. Sitting on edge of bed to supine Cannot perform the activity - 0  Can perform the activity with support from 2 persons  -1  Can perform the activity with support from 1 person  -2  Can perform the activity without any help -3  Retrieved from "https://www.physio-pedia.com/index.php?title=Modified_version_of_PASS&oldid=101055" Get Top Tips Tuesday and The Latest Physiopedia updates Email Address I give my consent to Physiopedia to be in touch with me via email using the information I have provided in this form for the purpose of news, updates and marketing. HP Yes please It's free, and you can unsubscribe any time. Privacy policy. Our Partners The content on or accessible through Physiopedia is for informational purposes only. Physiopedia is not a substitute for professional advice or expert medical services from a qualified healthcare provider. 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搜尋搜尋搜尋切換導航 pPhysiopedia pPhysiopedia 關於新聞貢獻課程資源商店聯繫登入 pPhysiopedia 關於新聞貢獻課程資源商店聯繫 p + 內容編輯者分類引用內容正在加載...編輯者正在加載...分類正在加載...引用資料時，在學術寫作中應盡量引用原始來源。通常這是信息首次被提出的期刊文章。在大多數情況下，Physiopedia 文章是次級來源，因此不應用作引用來源。Physiopedia 文章最好用於查找原始來源信息（請參閱文章底部的參考列表）。如果您認為此 Physiopedia 文章是您引用信息的原始來源，您可以使用以下按鈕訪問相關引用陳述。引用文章修改版本的 PASS 跳轉至：導航、搜尋 修改後的中風姿勢評估量表（PASS）[編輯 | 編輯源]每項僅允許一次嘗試。確保患者管理以下分數的標準，以及登記分數的標準。 一個計時器在第 4 項和第 7-9 項使用，患者需要在特定時間內維持姿勢。第 4 項應在患者腳部有支援的情況下進行。在第 1-3 項、第 5-6 項和第 10-12 項中，患者的姿勢平衡/控制應根據不同的支援程度進行評分。1. 仰躺轉向受影響側邊 不能完成活動 - 0 可在兩人支援下完成活動 - 1 可在一人支援下完成活動 - 2 可無支援下完成活動 - 3 2. 仰躺轉向非受影響側邊 不能完成活動 - 0 可在兩人支援下完成活動 - 1 可在一人支援下完成活動 - 2 可無支援下完成活動 - 3 3. 仰躺轉向床邊坐起 不能完成活動 - 0 可在兩人支援下完成活動 - 1 可在一人支援下完成活動 - 2 可無支援下完成活動 - 3 4. 無支援坐立 不能坐立 - 0 可在一小手支援下坐立 - 1 可坐立超過 10 秒無支援 - 2 可坐立 5 分鐘無支援 - 3 5. Sitting to standing up 不能完成活動 -0 可以在兩人支持下完成活動 -1 可以在一人支持下完成活動 -2 可以在無任何幫助下完成活動 -3 6. 有支持站立 不能站立，即使有支持 -0 可以在兩人強力支持下站立 -1 可以在一人支持下站立 -2 可以在一人手上支持下站立 -3 7. 無支持站立 不能站立無支持 -0 可以站立無支持十秒或倚靠一腿 -1 可以站立無支持超過一分鐘或站立稍微不對稱 -2 可以站立無支持超過一分鐘並同時從前手到頸部移動手/手臂，手臂平行於身體以避免疲勞 -3 8. 以非癱瘓腿站立 不能以非癱瘓腿站立 -0 可以以非癱瘓腿站立數秒 -1 可以以非癱瘓腿站立超過五秒 -2 可以以非癱瘓腿站立超過十秒 -3 9. 站立於偏瘫腿上 不能站立於非偏瘫腿上 -0 能夠站立於非偏瘫腿上數秒 -1 能夠站立於非偏瘫腿上超過 5 秒 -2 能夠站立於非偏瘫腿上超過 10 秒 -3 10. 站立並從地上拾起鞋子 不能執行該活動 -0 能夠在兩人支持下執行該活動 -1 能夠在一人支持下執行該活動 -2 能夠無任何幫助下執行該活動 -3 1. 由站立坐下 不能執行該活動 -0 能夠在兩人支持下執行該活動 -1 能夠在一人支持下執行該活動 -2 能夠無任何幫助下執行該活動 -3 12. Sitting on edge of bed to supine 不能執行該活動 - 0 可以在兩個人的支持下執行該活動 -1 可以在一人支持下執行該活動 -2 可以在無任何幫助下執行該活動 -3 取自 "https://www.physio-pedia.com/index.php?title=Modified_version_of_PASS&oldid=101055" Get Top Tips Tuesday 和 The Latest Physiopedia 更新 Email Address 我同意 Physiopedia 透過電子郵件與我聯繫，以提供新聞、更新和市場推廣資訊。HP 是免費的，您可以隨時退訂。隱私權政策。我們的合作伙伴 Physiopedia 上的內容僅供參考之用。Physiopedia 不是專業建議或合格醫療服務的替代品。 上讀更多 pPhysiopedia +Plus   Physiopedia 首頁 捐贈 購物 聯絡內容 文章 分類 資源 報告內容 計畫 貢獻 課程 法律聲明 使用條款 隱私權 Cookie 政策 版權所有 © Physiopedia 2025 | Physiopedia 是英國註冊慈善機構，登記編號：1173185 返回頂端 Upper-Crossed Syndrome - Physiopedia
上十字綜合症 - Physiopedia Introduction Upper crossed syndrome (UCS) is defined as altered muscle activation and movement patterns of the head, neck, shoulders and back muscles[1]Muscles of neck and chest like suboccipitalis, sternocleidomastoid (SCM), levator scapulae, pectoralis major and minor, scalenes, and upper trapezius (UT) become tight or short and muscles of neck and posterior upper back like deep neck flexors (DNFs), Serratus Anterior (SA), rhomboids, middle trapezius (MT), and lower trapezius (LT) become stretched, weak and restrained. Tightness and weakness are in a crossed pattern. The tightness of the suboccipitalis, levator scapulae, and UT on the dorsal side is crossed by the tightness of the pectoralis major and minor, SCM, and scalenes on the ventral side; the weakness of DNFs on the ventral side is crossed by the weakness of the SA, rhomboids, MT, and LT[1] This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment[2]. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighbouring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae. These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapulae and upper trapezius to increase activation to maintain glenohumeral centration[4]. Exposure of the human body to gravity forces, e.g., when standing or walking, is necessary to ensure proper activity of the skeletal muscles responsible for maintaining good body posture. When these muscles are not stimulated to resist gravity for an extended period, e.g., during prolonged sitting or lying, their stabilizing function is disturbed by the hypoactivity reaction resulting in muscular weakness and atrophy. The deficit of the locomotor system stability triggers a compensatory mechanism—the stabilizing function is overtaken by the mobilizing muscles. However, as a side effect, such compensation leads to mobilizers’ increased activity (hyperactivity) and, subsequently, their decreased flexibility, which may finally lead to a pathological chain of reactions within the musculoskeletal system[5][6][7][8][9][10]. Pathological Process[edit | edit source] Muscle balance can be defined as a relative equality of muscle length or strength between an agonist and an antagonist; this balance is necessary for normal movement and function[4].Muscle imbalance usually occurs before functional dysfunction[11]. The condition in which few muscles undergo inhibition and become weak while others become short and stiff can bring certain changes in the tissues which may cause inappropriate movement patterns. This can cause pain and inflammation Janda attributes these predicted patterns to a large extent, due to the immobile conditions and repetitive tasks[12][13]. In UCS, mainly the posterior superior muscles in the neck and the anterior neck, which are tonic, are short and the anterior deep muscles of the neck and posterior shoulder girdle, which are mainly phasic, are inhibited and weakened. This condition is caused by the changes in the elevation, protraction and abduction of the shoulder by increasing the angle of forward head and hyperextension of the upper part of the cervical spine, which are often associated with forward head, round shoulder, protracted scapulae, and thoracic kyphosis[12][13]. These muscle imbalances and movement dysfunctions may have a direct effect on joint surfaces, thus potentially leading to joint degeneration. In some cases, joint degeneration may be a direct source of pain, but the actual cause of pain has been often secondary to muscle imbalance[14]. Muscles may become unbalanced as a result of adaptation or dysfunction. Such muscle imbalances can be either functional or pathological: Functional muscle imbalances occur in response to adaptation for complex movement patterns, including imbalances in strength or flexibility of antagonistic muscle groups[4]. The structural approach focuses on actual damage to musculoskeletal structures such as rotator cuff tendonitis or a ligament injury. The functional approach examines factors that contribute to structural lesions. This approach is most useful for physical therapy management of chronic ‘dysfunctions’ such as persistent joint pain and tendonitis[15]. When muscle imbalance impairs function, it is considered to be pathological. Pathological muscle imbalance typically is associated with dysfunction and pain, although its cause may or may not result from an initial traumatic event. Pathological imbalance may also be insidious; many people have these muscle imbalances without pain. Ultimately, however, pathological muscle imbalance leads to joint dysfunction and altered movement patterns, which in turn lead to pain. Note that this muscle imbalance continuum may progress in either direction; muscle imbalance may lead to altered movement patterns and vice versa. Some injuries cause muscle imbalance, while others may result from muscle imbalance. Sometimes pathological imbalances are a functional compensation for an injury[4].For example, unbalanced biomechanical joint stresses that result from muscle imbalance may lead to joint damage, setting up a vicious cycle of pain and inflammation. The structural inflammation then affects the neuromuscular system of the joint, creating further dysfunction. Eventually, the body adapts the motor program for movement to compensate for the dysfunction. The functional cause of the problem is muscle imbalance, while the symptom is pain and inflammation resulting from a structural lesion. Therefore, it is possible to have both a structural and a functional lesion, but for accurate diagnosis and treatment, the clinician must decide which lesion is the actual cause of dysfunction[4]. Functional imbalance Pathological imbalance Atraumatic With or without trauma Adaptive change Adaptive change Activity specific Associated with dysfunction No pain With or without pain Proprioceptive senses are the senses used to control the positions and motions of the trunk and parts of the body in space[16]. Proprioceptive senses related to the spatial recognition of the head require not only information from the vestibular organs and visual information, but also proprioceptive sense information from the cervical spine[17]. Proprioceptive senses perform two important roles in the neck: they provide information on posture and motion of the cervical spine to the central nervous system, and they provide cervical reflexes for stability and protection of the cervical spine[18]. Pathology, injuries, muscle fatigue, and aging have been reported as causes of damage to cervical spine positional senses, and recent studies have reported that position sense declines in patients with damage to the cervical spine or who complain of pain[19][20]. Clinical Presentation[edit | edit source] Individuals who present with upper crossed syndrome will show a forward head posture (FHP), hunching of the thoracic spine-as well as changed function in the shoulder girdle, elevated and protracted shoulders, scapular winging, and decreased mobility of the thoracic spine[21][4]. FHP, round shoulder, and kyphosis are postural deviations including excessive neck protraction and thoracic spine flexion, anterior tilt, and downward rotation of scapula with an inclining tendency and internal rotation of shoulder[4].FHP is related to thoracic kyphosis[22].In addition, a relationship between the FHP and round shoulder as well as round shoulder and kyphosis has been reported[22]. However, it is not possible to determine which one is the cause and which one is the effect. In UCS, the head is laid in FHP[23]. Weak muscles: Lower and middle trapezius. Serratus anterior, decreased SA activity will be accompanied by a reduction in control of the scapula in static and dynamic states[24]. Infraspinatus Deep neck flexors, play a key role in maintaining the neck's posture. These muscles are weak and prolonged in people with FHP and are not properly recruited[25]. Tight muscles: Upper trapezius, increase in the UT activity increases the anterior tilt of the scapula and elevates it, leading to a decrease in subacromial space, which increases the probability of shoulder pathology[24]. Pectorals, tightness of the pectoralis major creates an anterior force on the glenohumeral joint with a consequent decrease in stability[26].A tight pectoralis minor limits scapular upward rotation, external rotation, and posterior tilt, thereby reducing SAS[27]. Levator scapulae, shortness of the levator scapulae may affect muscle coordination and increase shear force and compressive load in cervical spine[28]. Diagnostic Procedures[edit | edit source] In clinical practice, it is advisable to begin muscle evaluation by analyzing erect standing posture and gait. The c1inician is given an overall view of the patient's muscle function through posture and gait analysis and is challenged to look comprehensively at the patient's entire motor system and not to limit attention to the local level of the lesion[29].Muscle analysis of standing posture: posterior view, anterior view, lateral view[4]. Evaluation of balance[4]. Hipermobility[4]. Evaluation of muscle imbalance in a patient with an acute pain syndrome, however, is unreliable and must be undertaken with precaution. A precise evaluation of tight muscles and movement patterns can be performed only if the patient is pain-free or almost pain-free. Its usefulness is greatest in the chronic phase or in patients with recurrent pain after the acute episode has subsided[29]. Upper-Quarter Muscles[edit | edit source] The muscles of the upper quarter include those of the cervical spine, shoulder, and arm. The muscles prone to tightness are those involved in a protective flexor response. Tightness of the upper trapezius, pectoral muscles, and suboccipitals, in particular, is a hallmark sign of Janda's UCS[4]. Upper trapezius m.is tested with the patient supine, with the head passively flexed and side-bent to the contralateral side. Once the slack is taken up, the shoulder girdle is pushed distally. Normally, a sort barrier is felt at the end of the push; however, when the movement is restricted, the barrier has an abrupt firm to hard end-reel[29]. Levator scapulae m. is examined in a similar manner, except that the head is also rotated to the contralateral side[29]. Deep posterior neck m. muscles can be tested only by thorough palpation. Evaluation of the sternocleidomastoid is not reliable because it crosses too many segments[29]. Pectoralis major m. is tested with the patient supine. The trunk must be stabilized before the arm is placed into abduction because a possible twist of the trunk might mimic the normal range of movement. The arm should reach the horizontal level. To estimate the clavicular portion, the arm is allowed to hang down loosely and the examiner applies a posterior glide to the shoulder. Normally, only a slight soft barrier is felt[29]. V.Janda had suggested testing pectoralis major muscle. The different portions of the pectoralis major are tested separately. The clinician is able to target the specific portions by changing the amount of shoulder abduction. • Lower sternal fibers. The clinician abducts the patient's arm to 150° with slight external rotation. The normal length of these pectoral fibers allows the patient's arm to rest in a horizontal position; slight overpressure produces end-feel resistance. The clinician should also palpate the sternal fibers medial to the axilla for tenderness. Shortness or hypertonicity of the muscle is indicated by an inability of the arm to reach horizontal or a palpable tenderness in the muscle. • Midsternal fibers. The clinician abducts the patient's arm to 90° and palpates the muscle fibers at the second rib interspace. The normal length of these fibers allows the patient's arm to rest below the horizontal. There is gradual end-feel resistance when the clinician applies slight overpressure. Palpation does not produce tenderness. • Clavicular fibers. The clinician places the patient's arm in an extended position close to the body and allows the arm to come to a rest. The normal length of these fibers allows the patient's arm to rest below the horizontal. The clinician applies a gentle anteroposterior and caudal pressure through the glenohumeral joint as well as palpates the fibers just inferior to the clavicle. Resistance to this pressure should be gradual and fibers should not be tender to palpation[4]. Pectoralis Minor m. is tested with the patient supine. The clinician views the mark on the patient from a superior view. The normal distance between the acromion and the table is 1 in. The horizontal levels of the anterior aspects of the acromions can be compared with each other. The two acromions should be on the same level; a higher acromion indicates possible pectoralis minor tightness[4]. Latissimus Dorsi m. is tested with the patient supine. The clinician stands beside the arm being tested. The clinician passively elevates the patient's arm toward the head of the table. The normal length of the latissimus dorsi allows the arm to rest horizontally to the table with the lumbar spine flat on the table. Tightness of this muscle is indicated by the arm resting above horizontal or by the lumbar spine going into extension[4]. [30] Janda's Basic Movement Patterns[edit | edit source] Janda identified six basic movement patterns that provide overall information about a particular patient's movement quality and control; these movements form the basis of the hip extension, hip abduction, curl-up, cervical flexion, push-up, and shoulder abduction movement pattern tests. The clinician should observe both the left and right sides for comparison. Muscle or limb trembling during these tests is considered a positive finding, indicating weakness or fatigue. Some patients do not need to perform all six tests at once; the clinician should decide which tests are indicated based on the postural analysis and history[4]. Cervical Flexion Movement Pattern Test[edit | edit source] [31] Push-Up Movement Pattern Test[edit | edit source] [32] Shoulder Abduction Movement Pattern Test[edit | edit source] [33] Additional Movement Tests[edit | edit source] Craniocervical Flexion Test [34] Breathing Patterns[edit | edit source] The primary muscles responsible for respiration are the diaphragm, intercostals, scalenes, transverse abdominis (TrA), pelvic floor muscles, and deep intrinsic spinal muscles. Each of these muscles plays a role in both respiration and spinal stabilization. According to Kendall, McCreary, and Provance, of the 20 primary and accessory muscles associated with respiration, almost all of them have a postural function. Some patients may show relatively normal respiratory patterns when relaxed in a supine position but may change into accessory-muscle or chest breathers when challenged in a functional position such as sitting at a computer or standing erect. Thus respiration patterns should be assessed with the patient in various positions, especially any painful positions used in ADL. A simple test is for the clinician to gently rest her hands on the patient's shoulders during quiet breathing to note any upward movement of the shoulders that would indicate accessory respiration. There are several things to observe in assessing respiration: Initiation of breath - the initiation of breathing should be at the abdominal region and not the chest. Lateral excursion of the lower rib cage during inspiration - movement of the rib cage is best assessed with the patient in the seated or standing position. Upper-chest expansion during the final phase of inspiration - the most common faulty pattern is the superior or cranial excursion, or lifting of the upper ribs by the scalenes and upper trapezius to substitute for inefficient or inhibited diaphragm activity[4]. Hence, for the assessment of UCS, the alignment and its side effects are often evaluated, such as an increase in thoracic kyphosis or forward head angles, while less attention has been paid to the keystone, i.e., the scapulae, and the relevant altered muscle activation and movement patterns[35]. In this regard, many researchers and therapists have only evaluated one of the affected regions, such as head, shoulders, or spine, separately and reported a degree of postural deviation regardless of other relevant malalignments and patterns of the muscle activation and related movement patterns, such as scapulohumeral rhythm or neck flexion[36]. Outcome Measures[edit | edit source] Shoulder Pain and Disability Index (SPADI)[37] Neck Disability Index[38] Occiput to Wall Test SF-36 questionnaire[39] McGill-Melzack Pain Questionnaire[39] Visual analogue scale (VAS)[14] Management / Interventions[edit | edit source] Over recent decades, therapists have been seeking to design appropriate exercises to correct musculoskeletal malalignments mainly through structural and functional approaches[40][41][42]. In the traditional structural approach, the changes observed in malalignments such as in UCS are attributed to biomechanics and are presumed to lead to adjustments in the length and strength of local muscles[40][41]. This may account for the stretching of short muscles and strengthening of weakened muscles at the site of the problem in the correction phase while ignoring other related malalignments[43]. Interestingly, despite the popularity of this method, very little research has been conducted based on this theory[44]. Furthermore, some review studies have questioned the effectiveness of strengthening and stretching exercises to improve postural disorders[45]. Bayattork, M., Seidi, F., Minoonejad, H. et al. The effectiveness of a comprehensive corrective exercises program and subsequent detraining on alignment, muscle activation, and movement pattern in men with upper crossed syndrome: protocol for a parallel-group randomized controlled trial. Trials 21, 255 (2020). In contrast, the functional (neurological) approach to musculoskeletal problems is based on the interaction of the central and peripheral nervous systems, and the involvement of the muscular and skeletal structures in producing and controlling motion[46]. In this functional approach, the musculoskeletal problems are attributed to the role of muscles in motor function; furthermore, changes in the alignment result not only from changes in muscle length and strength but also from more important changes in muscle neuromuscular factors, such as muscle recruitments[42]. In fact, the motor control unit may change the muscle activation strategy for temporary stabilization due to the presence of dysfunction. These changes in motor recruitment will alter the muscular balance, movement patterns, and eventually the motor program[41]. Similarly, Hodges et al. noted that motor control interventions require tailoring to each individual’s posture, muscle activation, and movement pattern[47]. There have been some studies showing effective exercise programmes for people with UCS, and one of these is Comprehensive corrective exercise program (CCEP)[48], Below is the list of exercises used in the CCEP: Each exercise session begins with 10 min of warm-up activity and ends with 5 min of cool-down. Selected exercises are designed in three phases: initial, improvement, and maintenance. The initial phase exercises (Fig. 3)[48] include laying supine on a foam roll in three different arm abduction angles (exercise 1A–C), side-lying external rotation (exercise 2), side-lying forward flexion (exercise 3), standing diagonal flexion (exercise 4), and military press (exercise 5). Participants with less ability can do exercises 4 and 5 in a sitting position. Once a participant regains muscle balance in the static conditions, he will try to add upper extremity movements in exercise positions. Exercises progress in frequency and intensity during this phase, as long as participants are able to demonstrate good quality movement. The initial phase duration is 2 weeks and the exercises will be performed for seven sets of 10-s hold to ten sets of 15-s hold. The goal of the improvement phase is to create the necessary tissue adaptations in the participant. Therefore, during this phase Thera-Bands, weights, and training balls will be used. Improvement phase exercises (Fig. 4) include side-lying external rotation with a dumbbell (exercise 6), side-lying forward flexion with a dumbbell (exercise 7), standing diagonal flexion with a dumbbell (exercise 8), standing external rotation with Thera-band (exercise 9), standing diagonal flexion with Thera-band (exercise 10), abduction in sitting on a training ball (exercise 11), lying prone V, T, and W exercises (exercise 12), and abduction in standing on a balance board (exercise 13). Exercises are progressed by considering individual characteristics of each participant and by observing the overload principle and the progression in the number of repetitions of each set during the 4 weeks of the improvement phase. The exercises will be performed from five sets of ten repetitions to six sets of 15 repetitions. Maintenance phase exercises: The exercises are the same as in the improvement phase without any progression in intensity and frequency. The maintenance phase duration is 2 weeks[48]. V. Janda firmly believed that the CNS and motor system function as one unit, the sensorimotor system. He suggested treatment be organized into three stages: Normalization of the peripheral structures. All peripheral structures outside the CNS must be treated in order to improve the quality of afferent information being received by the CNS. Central Indirect Technique: Vojta approach, and Feldenkrais. Local Direct Techniques: soft-tissue techniques, neural tension techniques and neurodynamics, joint mobility techniques and others. Restoration of muscle balance. The balance between the phasic and tonic muscle systems must be improved as a prerequisite for improving coordination. Facilitation of afferent system and sensory motor training. This training improves movement coordination and therefore promotes ideal mechanical loading of biological structures and efficient motor execution[4]. Other Science-Based Evidence Articles[edit | edit source] Apoorva Phadke et al. in the study has concluded muscle energy technique was better than stretching technique in improving pain and functional disability in people with mechanical neck pain[49]. Rasoul Arshadi et al. in the study has concluded eight week corrective exercises balance muscles activity and can be used to manage developing upper quadrant musculoskeletal disorders in person with UCS[50]. Arshadi, R.et al. in the study has concluded eight week corrective exercise succeeded in decreasing activity of SCM and UT muscles, UT/SA and UT/LT ratio, increasing activity of SA and LT. With regard to observing the large effects it can be stated corrective exercise (stretching, strengthening, and stabilization exercises) is a safe and low-cost way to optimize the muscles of the upper quadrant. Corrective exercises can be suggested as an effective modality to restore and maintain balanced muscle activity in people with UCS[50]. Differential Diagnosis[edit | edit source] Scheuermann's Kyphosis Stress and anxiety Pseudoradicular syndrome Scalene syndrome
Introduction 上交叉症候群（UCS）被定義為頭、頸、肩和背部肌肉的肌肉激活和運動模式異常[1]頸部和胸部的肌肉如頸後小肌、胸鎖乳突肌（SCM）、提肩肌、大肌群和小肌群、鎖骨下肌和上斜方肌（UT）變得緊繃或短縮，而頸部和上背部的肌肉如深頸屈肌（DNFs）、前鋸肌（SA）、菱形肌、中斜方肌（MT）和下斜方肌（LT）則變得拉長、疲弱和受限。緊繃和疲弱呈交叉模式。背側的頸後小肌、提肩肌和 UT 的緊繃與腹側的大肌群、SCM 和鎖骨下肌的緊繃交叉；DNFs 的腹側疲弱與 SA、菱形肌、MT 和 LT 的疲弱交叉[1]這種不平衡的模式會造成關節功能障礙，特別是在枕寰關節、C4-C5 段、頸胸關節、肩鎖關節和 T4-T5 段[2]。Janda 注意到這些脊柱中的焦點壓力區域對應於鄰近椎體形態轉換的轉換區。 特定的姿勢改變在 UCS 中可以看到，包括前傾頭部姿勢、增加的頸椎 lordosis 和胸椎 kyphosis、抬高的前伸肩膀，以及肩胛骨的旋轉或外展和飛翼狀。這些姿勢改變會減少肩鎖關節的穩定性，因為由於 serratus anterior 的弱化，肱骨頭的凹陷變得更加垂直，導致肩胛骨的外展、旋轉和飛翼狀。這種穩定性的損失需要提肌和上斜方肌增加活化以維持肩鎖關節的中心化[4]。人類體位暴露於重力力，例如站立或行走，是確保維持良好姿勢的骨骼肌活動的必要條件。當這些肌肉在長時間不被刺激以抵抗重力時，例如在長時間坐著或躺著的情況下，其穩定功能會因低活動反應而受到干擾，導致肌肉弱化和萎縮。運動系統穩定性的不足觸發了一種代償機制——穩定功能由活動肌接管。 然而，作為副作用，這種補償會導致促動肌的活動增加（過度活躍），隨後其柔軟度降低，最終可能導致肌肉骨骼系統中的病理反應鏈[5][6][7][8][9][10]。病理過程[編輯 | 編輯源]肌肉平衡可以定義為拮抗肌和協同肌之間相對的肌肉長度或力量的平等；這種平衡對於正常的運動和功能是必要的[4]。肌肉不平衡通常發生在功能失常之前[11]。當少數肌肉受到抑制而變弱，而其他肌肉變短和僵硬時，可能會引起某些組織的改變，從而導致不適當的運動模式。這可能會引起疼痛和發炎。Janda 從很大程度上歸因於這些預測模式，由於固定條件和重複任務[12][13]。在 UCS 中，主要是在頸部後上部的促動肌短縮，而頸部前部的促動肌和後肩帶的主要機能肌被抑制和變弱。 此條件是由肩部的抬高、前伸和外展變化所引起，增加前傾頭部的角度和上頸椎脊椎的過伸，這些變化通常與前傾頭部、圓肩、前伸的肩胛骨和胸椎後凸有關[12][13]。這些肌肉不平衡和運動功能障礙可能會直接影響關節表面，從而可能導致關節退化。在某些情況下，關節退化可能是疼痛的直接來源，但疼痛的實際原因往往是由於肌肉不平衡[14]。肌肉不平衡可能是由於適應或功能障礙所導致。這種肌肉不平衡可以是功能性的或病理性的：功能性肌肉不平衡是對複雜運動模式適應的結果，包括拮抗肌群的力量或柔韌性不平衡[4]。結構性方法專注於實際損傷的肌肉骨骼結構，如肩袖肌腱炎或韌帶損傷。功能方法則探討導致結構性病變的因素。 This approach 最有用於處理慢性「功能障礙」如持續性關節疼痛和肌腱炎的物理治療管理[15]。當肌肉不平衡影響功能時，就被視為病理性的。病理性的肌肉不平衡通常與功能障礙和疼痛有關，雖然其原因可能是或可能不是由初始的外傷事件引起的。病理性的不平衡也可能是漸進的；很多人有這些肌肉不平衡而沒有疼痛。然而，最終，病理性的肌肉不平衡導致關節功能障礙和運動模式改變，這又導致疼痛。請注意，這種肌肉不平衡的連續過程可能朝兩個方向進行；肌肉不平衡可能導致運動模式改變，反之亦然。有些傷害導致肌肉不平衡，而其他傷害則可能是由肌肉不平衡引起的。有時，病理性的不平衡是對傷害的功能性補償[4]。例如，由肌肉不平衡引起的不均衡生物力學關節壓力可能會導致關節損傷，形成疼痛和發炎的惡性循環。結構性的發炎然後影響關節的神經肌肉系統，進一步造成功能障礙。 Eventually，身體適應運動的運動程式以補償功能障礙。問題的功能原因是肌肉不平衡，而症狀則是來自結構性損傷的疼痛和發炎。因此，有可能同時存在結構性和功能性損傷，但為了準確診斷和治療，臨床醫生必須決定哪種損傷是功能障礙的实际原因[4]。功能不平衡 病理性不平衡 無外傷 有或無外傷 适应性改變 适应性改變 活動特定 与功能障碍相关 無痛 有或無痛 本體感受器是用來控制身體各部位在空間中的位置和運動的感覺[16]。本體感受器與頭部空間識別相關的信息不僅來自前庭器官和視覺信息，還來自頸椎的本體感受器[17]。 proprioceptive 嗅覺在頸部扮演兩個重要角色：它們向中樞神經系統提供颈椎姿勢和運動的信息，並提供颈椎反射以維持穩定性和保護颈椎。病理、傷害、肌肉疲勞和老化已被報告為導致颈椎位置感受损的原因，最近的研究報告指出，颈椎損傷或主訴疼痛的患者的位置感會下降[18]。臨床表現[編輯 | 編輯源代码] 出現上交叉綜合徵的個體將顯示前傾頭姿態（FHP）、胸椎前凸，以及肩帶功能改變，包括肩胛骨上提和前伸、肩胛骨飛翼狀以及胸椎活動度下降[21][4]。 FHP,圓肩和 kyphosis 是姿態偏移，包括頸部前伸和胸椎前彎曲、前傾和肩胛骨前傾及內旋[4]。FHP 與胸椎 kyphosis 相關[22]。此外，FHP 與圓肩以及圓肩與 kyphosis 之間的關係已被報告[22]。然而，無法確定哪個是原因，哪個是結果。在 UCS 中，頭部位於 FHP[23]。弱肌肉：下和中斜方肌。前鋸肌，減少 SA 活動將伴隨著在靜態和動態狀態下對肩胛骨控制的減少[24]。內旋肌、深頸屈肌，在維持頸部姿態中扮演關鍵角色。這些肌肉在 FHP 的人身上較為緊繃且長期處於緊張狀態，並未適當募集[25]。緊肌肉：上斜方肌，UT 活動增加會增加肩胛骨前傾並抬高它，導致肩峰下空間減少，增加肩部病理的機率[24]。 pectorals, 胸大肌緊繃會在肱鎖關節產生前方力，從而導致穩定性下降[26]。緊繃的胸小肌限制了肩胛骨的向上旋轉、外旋和後傾，從而減少 SAS[27]。提肩肌，提肩肌短縮可能影響肌肉協調並增加颈椎的剪切力和壓縮負荷[28]。診斷程序[編輯 | 編輯源] 在臨床實踐中，建議從分析站立姿勢和步態開始進行肌肉評估。臨床醫生通過姿勢和步態分析可以獲得患者肌肉功能的整體視圖，並被挑戰著全面評估患者的整個運動系統，而不要僅限於局部病變的關注[29]。站立姿勢的肌肉分析：後方視圖，前方視圖，側方視圖[4]。平衡評估[4]。然而，對於急性疼痛綜合徵患者的肌肉不平衡評估是不可靠的，必須謹慎進行。 緊密肌肉和運動模式的精確評估只有在患者無痛或幾乎無痛時才能進行。其最有效的應用是在慢性期或急性發作後反復疼痛的患者身上[29]。上肢肌肉[編輯 | 編輯源] 上肢肌肉包括頸椎、肩部和手臂的肌肉。容易緊繃的肌肉是參與保護性屈曲反應的肌肉。特別是上斜方肌、胸大肌和頸後部肌肉的緊繃是 Janda 的上肢肌肉失調綜合徵的典型症狀[4]。上斜方肌 m.的測試是在患者仰臥位時進行，頭部被動屈曲並向對側側傾。一旦鬆弛被消除，肩帶被推向下。正常情況下，在推壓的末端會感到一種阻力；然而，當運動受限時，阻力的終端會突然變為堅硬[29]。肩胛提肌 m.的檢查方法類似，只是頭部還向對側旋轉[29]。深層後頸肌群只能通過仔細觸摸來測試。 評估胸鎖乳突肌並不可靠，因為它跨越了太多節段[29]。胸大肌 m.是在患者仰臥時測試的。在放置手臂於外展之前必須穩定軀幹，因為軀幹可能的扭轉可能會模仿正常的活動範圍。手臂應達到水平位置。為了估計鎖骨部分，手臂可以鬆鬆地垂下，檢查員對肩部施以後方滑動。正常情況下，只能感受到輕微的軟障礙[29]。V.詹達曾建議測試胸大肌肌肉。胸大肌的不同部分應分別測試。臨床醫生可以通過改變肩部外展的程度來針對特定部分。• 下胸骨纖維。臨床醫生將患者的手臂外展至 150°並伴有輕微的外旋。這些胸肌纖維的正常長度允許患者的手臂位於水平位置；輕微的過度壓力會產生終端阻力感。臨床醫生還應觸摸腋下內側的胸骨纖維以檢查是否有壓痛。 肌肉的短縮或肌張力增高會表現為手臂無法伸直至水平，或可觸及肌肉的壓痛。• 中胸肌纖維。 Clinician 使患者手臂向外展至 90°，並於第二肋間間隙處觸診肌肉纖維。這些纖維的正常長度允許患者的手臂位於水平之下。當 Clinician 施加輕微的過度壓力時，會有漸進的阻力感。觸診不會引發壓痛。• 肋鎖肌纖維。 Clinician 使患者手臂伸直靠近身體，並讓手臂自然休息。這些纖維的正常長度允許患者的手臂位於水平之下。Clinician 施加輕微的前後及向下壓力於肩鎖關節，並觸診鎖骨下方的肌肉纖維。對此壓力的阻力應漸進，且肌肉纖維不應在觸診時感到壓痛[4]。胸小肌的測試是在患者仰臥時進行。Clinician 從上方觀看患者。正常情況下，肩峰與床面之間的距離為 1 英寸。 前銳邊的水平可以相互比較。兩個銳邊應該在同一水平；較高的銳邊可能表示胸小肌緊繃[4]。背阔肌的測試是在患者仰臥時進行。臨床醫生站在被測試手臂旁邊。臨床醫生將患者的手臂 Passively 向上抬向床頭。正常情況下，背阔肌的長度允許手臂水平放置於床上，而腰椎平躺在床上。此肌肉緊繃會表現為手臂超過水平或腰椎進入伸展[4]。[30] Janda 的基本運動模式[編輯 | 編輯源] Janda 識別了六種基本運動模式，這些模式提供了關於患者運動品質和控制的總體信息；這些運動是骨盆後伸、骨盆外展、卷腹、頸部前屈、俯卧撐和肩部外展運動模式測試的基礎。臨床醫生應觀察左右兩側進行比較。這些測試中肌肉或肢體顫抖被視為陽性發現，表示弱點或疲勞。 有些患者不需要一次進行六項測試；臨床醫生應根據姿勢分析和病史決定哪些測試是必要的[4]。頸部屈曲運動模式測試[編輯 | 編輯源] [31]推舉運動模式測試[編輯 | 編輯源] [32]肩部外展運動模式測試[編輯 | 編輯源] [33]額外的運動測試[編輯 | 編輯源]頭頸部屈曲測試 [34]呼吸模式[編輯 | 編輯源]主要負責呼吸的肌肉包括膈肌、肋間肌、斜角肌、橫膈肌（TrA）、骨盆底肌肉和深層固有脊柱肌肉。這些肌肉在呼吸和脊柱穩定中都扮演著角色。根據肯德林、麥克雷和普羅凡斯的說法，與呼吸相關的 20 個主要和輔助肌肉中，幾乎所有肌肉都有姿勢功能。有些患者在仰臥放鬆時可能顯示出相對正常的呼吸模式，但在進行功能位置如坐在電腦前或直立站立時，可能會轉變為輔助肌肉或胸式呼吸。 因此，呼吸模式應在患者不同姿勢下評估，特別是在進行 ADL 時使用的任何疼痛姿勢。一個簡單的測試是讓臨床人員輕輕將手放在患者肩膀上，在安靜呼吸時注意肩部是否有向上移動，這會表明輔助呼吸。評估呼吸時需要注意幾點：呼吸的啟動應在腹部而非胸部。吸氣時下肋骨側向移動 - 最好在患者坐著或站立時評估肋骨的移動。吸氣最終階段上胸部擴張 - 最常見的錯誤模式是上部或頭部移動，或由斜角肌和上斜方肌提升上肋骨以代替無效或受抑制的膈肌活動[4]。 故此，對於 UCS 的評估，通常會評估其對齊情況及其副作用，例如胸椎後凸或前傾角度的增加，而對鍵石，即肩胛骨及其相關改變的肌肉激活和運動模式則關注較少[35]。在此方面，許多研究人員和治療師僅單獨評估受影響區域之一，如頭部、肩膀或脊柱，並報告了一定程度的姿勢偏移，而不考慮其他相關的對齊問題和肌肉激活及相關運動模式，例如肩鎖關節節律或頸部前屈[36]。結果指標[編輯 | 編輯源]肩痛和功能障礙指數（SPADI）[37]頸部功能障礙指數[38]枕骨至牆測試 SF-36 問卷[39]麥基爾-梅爾扎克疼痛問卷[39]視覺類比量表（VAS）[14]管理 / 干預措施[編輯 | 編輯源]近年來，治療師一直在尋求設計適合的運動來糾正骨骼肌肉的對齊問題，主要通過結構性和功能性的方法[40][41][42]。 在傳統結構方法中，如在上交叉綜合症（UCS）中觀察到的錯位變化被歸因於生物力學，並假設這些變化會導致局部肌肉長度和強度的調整[40][41]。這可能解釋了在糾正階段，短肌肉被拉伸和弱化肌肉被強化的情況，而忽略了其他相關的錯位[43]。有趣的是，儘管這種方法非常流行，但基於這種理論的研究卻非常少[44]。此外，一些綜述研究質疑強化和拉伸運動對改善姿勢障礙的有效性[45]。Bayattork, M., Seidi, F., Minoonejad, H. 等人. 上交叉綜合症患者全面糾正運動程序及其後的去訓練對對齊、肌肉激活和運動模式的影響：平行組隨機對照試驗的方案。Trials 21, 255 (2020)。 在相對而言，功能（神經學）對肌肉骨骼問題的處理方法是基於中樞神經系統和周圍神經系統的交互作用，以及肌肉和骨骼結構在產生和控制運動中的參與[46]。在這種功能方法中，肌肉在運動功能中的作用被歸因於肌肉骨骼問題；此外，姿勢的改變不僅來自於肌肉長度和強度的變化，還來自於更為重要的神經肌肉因素的變化，例如肌肉募集[42]。事實上，運動控制單元可能會因功能障礙的存在而改變肌肉激活策略以進行臨時穩定。這些神經肌肉募集的變化將改變肌肉平衡、運動模式，最終改變運動程序[41]。同樣，霍德奇斯等人指出，運動控制干預需要根據每個個體的姿勢、肌肉激活和運動模式進行量身定制[47]。 有一些研究顯示對於 UCS 患者有效的運動計劃，其中之一是全面糾正運動計劃（CCEP）[48]。以下是 CCEP 中使用的運動清單：每次運動會開始進行 10 分鐘的暖身活動，並結束於 5 分鐘的冷卻。選定的運動被設計成三個階段：初始、改善和維持。初始階段運動（圖 3）[48] 包括仰躺於泡沫滾筒上，手臂伸展角度不同的三種姿勢（運動 1A–C），側躺外旋（運動 2），側躺前屈（運動 3），站立對角屈曲（運動 4），以及軍事推舉（運動 5）。運動能力較弱的參與者可以坐在姿勢下進行運動 4 和運動 5。一旦參與者在靜態條件下恢復肌肉平衡，他將嘗試在運動姿勢中加入上肢運動。此階段運動的頻率和強度會逐步增加，只要參與者能夠展示出良好的運動質量即可。初始階段持續 2 周，運動將進行七組 10 秒的保持，至十組 15 秒的保持。 改善階段的目標是為參與者創造必要的組織適應。因此，在此階段將使用 Thera-Bands、重量和訓練球。改善階段的運動（圖 4）包括側臥外旋舉鈔桿（運動 6）、側臥前屈舉鈔桿（運動 7）、站立對角屈曲舉鈔桿（運動 8）、站立外旋使用 Thera-band（運動 9）、站立對角屈曲使用 Thera-band（運動 10）、坐於訓練球上舉（運動 11）、俯卧 V、T、W 運動（運動 12），以及站立於平衡板上舉（運動 13）。運動將根據每位參與者的個別特徵進行進階，並考慮超載原則，以及在 4 週的改善階段中每組次數的進階。運動將從每組十次進行五組，進階至每組十五次進行六組。維持階段運動：運動與改善階段相同，無任何強度和頻率的進階。維持階段持續 2 週[48]。V。 Janda 堅信神經系統和運動系統是一體的，組成 SENSORIMOTOR 系統。他建議治療分為三個階段：周圍結構的正常化。所有位於神經系統之外的周圍結構都必須治療，以改善傳送到神經系統的感覺信息質量。中央間接技術：Vojta 方法和費爾登克雷茨。局部直接技術：軟組織技術、神經張力技術和神經動力學、關節活動技術和其他方法。肌肉平衡的恢復。必須改善協調的前提是改善協調。感覺運動系統的促進和訓練。這種訓練改善運動協調，從而促進生物結構的理想機械負荷和有效的運動執行[4]。其他科學證據文章[編輯 | 編輯源] 阿波羅瓦·法德克等人的研究結論是，肌肉能量技術在改善機械性頸痛患者疼痛和功能障礙方面比拉伸技術更有效[49]。拉索爾·阿爾沙迪等。 在研究中已結論八週的校正運動可以平衡肌肉活動，並可用於管理具有 UCS 的人上 Quarter 肌肉骨骼疾病[50]。Arshadi, R.等人在研究中已結論八週的校正運動成功地減少了 SCM 和 UT 肌肉的活動，UT/SA 和 UT/LT 比率，並增加 SA 和 LT 的活動。考慮到觀察到的大型效果，可以說校正運動（伸展、強化和穩定性運動）是一種安全且低成本的方法，用於優化上 Quarter 的肌肉。校正運動可以建議作為恢復和維持平衡肌肉活動的有效方法[50]。差別診斷[編輯 | 編輯源] Scheuermann's Kyphosis Stress and anxiety Pseudoradicular syndrome Scalene syndrome Pressure Ulcer Scale For Healing (PUSH) - Physiopedia Introduction Once a pressure ulcer is identified, it should be staged and the wound size carefully documented. Additional assessments of the ulcer include its location, surrounding skin condition, presence of tissue undermining and tunneling, and amount of exudate, odour and tenderness.[1] Pressure Ulcer Scale for Healing (PUSH)[edit | edit source] The pressure ulcer scale for healing (PUSH) is a widely used tool developed by the National Pressure Ulcer Advisory Panel (NPUAP) that grades pressure ulcers based on wound size, wound bed tissue type, and exudate amount.[1] The PUSH provides a reliable measure of pressure ulcer healing over time and accurately distinguishes between healing and nonhealing ulcers. When used at weekly intervals, it is a clinically useful, evidence-based tool for tracking changes in pressure ulcer status.[2] Characteristics and directions for scoring[edit | edit source] Examine the pressure ulcer well and do not guess. Length x Width: Using a centimetre ruler, measure the greatest length (head to toe) and greatest width (side to side). Multiply these two measurements (length x width) to get a surface area estimate in square centimetres. (cm2). Exudate Amount: Assess the amount of drainage present after removing the dressing. Exudate should be estimated as none, light, moderate, or heavy. Tissue type: refers to the various types of tissue found in the wound (ulcer) bed. Score a "4" if necrotic tissue is present. If there is any slough present and necrotic tissue is absent, give it a 3. Score a "2" if the wound is clean and contains granulation tissue. A superficial wound that is reepithelializing receives a "1" score. Give it a "0" when the wound is healed. [3] Resources[edit | edit source] The National Pressure Injury Advisory Panel (NPIAP) Pressure Ulcer Scale for Healing (PUSH) PUSH Tool 3.0
Introduction 一經發現壓瘡，應進行分期並仔細記錄傷口大小。此外，還應評估壓瘡的位置、周圍皮膚狀況、是否存在組織塌陷和隧道現象，以及分泌物、臭味和痛感。[1] 壓瘡愈合量表（PUSH）[編輯 | 編輯源區] 壓瘡愈合量表（PUSH）是由國家壓瘡顧問委員會（NPUAP）開發的廣泛使用的工具，根據傷口大小、傷床組織類型和分泌物量對壓瘡進行分級。[1] PUSH 提供了一種可靠的壓瘡愈合時間測量方法，並能準確區分愈合和未愈合的壓瘡。每隔一周使用一次，它是一種臨床上有用的、以證據為基礎的工具，用於追蹤壓瘡狀態的變化。[2] 特徵和評分方向[編輯 | 編輯源區] 詢查壓瘡時要仔細觀察，不要猜測。長度 x 寬度：使用公分尺測量傷口的最大長度（頭到腳）和最大寬度（側向）。將這兩個測量值相乘（長度 x 寬度）以獲得平方公分的表面積估計值。（cm2）。 渗出物量：移除敷料後，評估滲出物的量。滲出物應估計為無、輕度、中度或重度。組織類型：指傷口（潰瘍）床中發現的各種組織類型。若存在壞死組織，評分為 4。若有鬆解組織且無壞死組織，評分為 3。若傷口乾淨且含有新生肉芽組織，評分為 2。若為表層傷口且正在重新上皮化，評分為 1。若傷口已愈合，則評分為 0。[3] 資源[編輯 | 編輯來源] 全國壓力損傷顧問小組（NPIAP）壓力潰瘍癒合量表（PUSH）PUSH 工具 3.0

References  參考資料[edit | edit source]

  1. ↑ Jump up to: 1.0 1.1 (Davies PM. Steps to Follow: A Guide to the Treatment of Adult Hemiplegia. New York, NY: Springer;1985)
    ↑ Jump up to: 1.0 1.1 (戴維斯 PM. 步驟指南：成人半身不遂的治療方法。紐約，紐約：斯普林格；1985)
  2. ↑ Jump up to: 2.0 2.1 2.2 Santos-Pontelli TEG, Pontes-Neto OM, de Araujo DB, Santos AC, and Leite JP. Persistent pusher behavior after a stroke. Clinics (Sao Paulo). 2011; 66(12): 2169–2171.
    ↑ Jump up to: 2.0 2.1 2.2 桑托斯-蓬特利 TEG, 桐特斯-內托 OM, 阿拉烏約 DB, 桑托斯 AC, 和 利特爾 JP。中風後持續的推者行為。 Clinics (聖保羅)。2011; 66(12): 2169–2171。
  3. ↑ Nolan J, Jacques A, Godecke E, Abe H, Babyar S, Bergmann J, Birnbaum M, Dai S, Danells C, Edwards TG, Gandolfi M. Post-stroke lateropulsion terminology: pushing for agreement amongst experts. Annals of Physical and Rehabilitation Medicine. 2022 Nov 1;65(6):101684.[1]
    ↑Nolan J, Jacques A, Godecke E, Abe H, Babyar S, Bergmann J, Birnbaum M, Dai S, Danells C, Edwards TG, Gandolfi M. 剛中癱後側推術語：專家之間達成共識的推動。Annals of Physical and Rehabilitation Medicine。2022 年 11 月 1 日；65(6):101684。[1]
  4. ↑ Karnath H, Ferber S, and Dichgans J: The origin of contraversive pushing. Evidence for a second graviceptive system in humans. Neurology 55(9): 1298, 2000.
    ↑卡納特 H, 費爾伯 S, 和 西格納斯 J: 交叉推舉的起源。人類存在第二個重力感受系統的證據。神經學 55(9): 1298, 2000.
  5. ↑ Pardo V, Galen S. Treatment interventions for pusher syndrome: A case series. NeuroRehabilitation. 2019 Jan 1;44(1):131-40.
    ↑帕爾多 V, 加倫 S. 推舉癥狀的治療干預措施：案例系列。神經康復. 2019 年 1 月 1 日;44(1):131-40.
  6. ↑ Perennou DA, Amblard B, Laassel el M, et al. Understanding the pusher behavior of some stroke patients with spatial deficits: a pilot study. Arch Phys Med Rehabil. 2002;83:570-575.
    ↑Perennou DA, Amblard B, Laassel el M, et al. 理解一些空間缺陷腦中風患者推舉行為：一項初步研究。Arch Phys Med Rehabil. 2002;83:570-575.
  7. ↑ Pedersen PM, Wandel A, Jorgensen HS, et al. Ipsilateral pushing in stroke: incidence, relation to neuropsychological symptoms, and impact on rehabilitation—the Copenhagen stroke study. Arch Phys Med Rehabil.1996 ;77:25–28
    ↑Pedersen PM, Wandel A, Jorgensen HS, et al. 腔隙性推移在中風患者中的發生率、與神經心理症狀的關係及對康復的影響—哥本哈根中風研究。Arch Phys Med Rehabil.1996 ;77:25–28
  8. ↑ Roller M. The ‘Pusher Syndrome. Journal of Neurological Physical Therapy. 2004; 28 (1): 29-34
    ↑Roller M. 《推手綜合徵》. 神經學物理治療雜誌. 2004; 28 (1): 29-34
  9. ↑ Danells CJ, Black SE, Gladstone DJ, McIlroy WE. Poststroke “pushing” Natural history and relationship to motor and functional recovery. Stroke. 2004 Dec 1;35(12):2873-8.
    ↑Danells CJ, Black SE, Gladstone DJ, McIlroy WE. 中風“推進”現象的自然病程及其與運動和功能恢復的關係。Stroke. 2004 年 12 月 1 日;35(12):2873-8.
  10. ↑ Jump up to: 10.0 10.1 10.2 Karnath HO, Johannsen L, Broetz D, Küker W. Posterior thalamic hemorrhage induces “pusher syndrome”. Neurology. 2005 Mar 22;64(6):1014-9.
    ↑ Jump up to: 10.0 10.1 10.2 卡爾納特 HO, 約翰森 L, 布雷茨 D, 克克爾 W。後部丘腦出血引發「推者症候群」。 神經學。2005 年 3 月 22 日;64(6):1014-9。
  11. ↑ Torrico TJ, Munakomi S. Neuroanatomy, Thalamus. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542184/
    ↑托里科 TJ, 極地 S。神經解剖學，丘腦。 [更新於 2022 年 7 月 25 日] 在：StatPearls [互聯網]。佛羅里達州塔斯瑞斯島：StatPearls 出版；2023 年 1 月-。可從：https://www.ncbi.nlm.nih.gov/books/NBK542184/
  12. ↑ Deecke L, Schwarz DW, Fredrickson JM. Nucleus ventroposterior inferior (VPI) as the vestibular thalamic relay in the rhesus monkey I. Field potential investigation. Experimental brain research. 1974 Apr;20:88-100.
    ↑Deecke L, Schwarz DW, Fredrickson JM. 猴子中下外側核（VPI）作為前庭丘腦傳導路徑的核團 I. 網格電位研究。實驗大腦研究。1974 年 4 月;20:88-100.
  13. ↑ Buttner U, Henn V. Thalamic unit activity in the alert monkeys during natural vestibular stimulation. Brain research. 1976.
    ↑Buttner U, Henn V. 在警覺猴子自然前庭刺激期間的丘腦單元活動。大腦研究。1976。
  14. ↑↑ Jump up to: 14.0 14.1 14.2 Paci M, Baccini M, Rinaldi LA. Pusher behaviour: a critical review of controversial issues. Disability and rehabilitation. 2009 Jan 1;31(4):249-58
    ↑ Jump up to: 14.0 14.1 14.2 @3# Paci M, Baccini M, Rinaldi LA. 推行行為：對爭議問題的關鍵評估。殘疾與康復。2009 年 1 月 1 日;31(4):249-58。
  15. ↑↑ Jump up to: 15.0 15.1 Babyar SR, Peterson MG, Bohannon R, Pérennou D, Reding M. Clinical examination tools for lateropulsion or pusher syndrome following stroke: a systematic review of the literature. Clin Rehabil. 2009;23:639-650.
    ↑ Jump up to: 15.0 15.1 Babyar SR, Peterson MG, Bohannon R, Pérennou D, Reding M. 險斜或推行症候群的臨床檢查工具：中風後文獻系統評估。臨床康復。2009;23:639-650。
  16. ↑↑ Jump up to: 16.0 16.1 16.2 16.3 Kim CS, Seok-Hyun Nam PT. Neurophysiological and Clinical Features of the Pusher Syndrome. Journal of Korean Physical Therapy. 2010 Jun 25;22(3):45-8.
    ↑ Jump up to: 16.0 16.1 16.2 16.3 Kim CS, Seok-Hyun Nam PT. 推行症候群的神經生理學和臨床特徵。韓國物理治療期刊。2010 年 6 月 25 日;22(3):45-8。
  17. ↑ Jump up to: 17.0 17.1 Abe H, Kondo T, Oouchida Y, Suzukamo Y, Fujiwara S, Izumi SI. Prevalence and length of recovery of pusher syndrome based on cerebral hemispheric lesion side in patients with acute stroke. Stroke. 2012 Jun 1;43(6):1654-6
    ↑ Jump up to: 17.0 17.1 阿本 H, 葛東 T, 臼井 Y, 須木摩 Y, 菊原 S, 知見 SI. 腦半球病變側別急性中風患者推車症狀之盛行率及恢復長度. 血管病學. 2012 年 6 月 1 日;43(6):1654-6
  18. ↑ Jump up to: 18.0 18.1 18.2 18.3 18.4 Karnath HO and Broetz D. Understanding and Treating “Pusher Syndrome. Physical Therapy. 2003;83:12:1119-1125
    ↑ Jump up to: 18.0 18.1 18.2 18.3 18.4 卡恩霍 HO 和 布羅茨 D. 理解並治療「推車症狀」. 物理治療. 2003;83:12:1119-1125
  19. ↑ Karnath HO, Ferber S, Dichgans J. The Origin of Contraversive Pushing: Evidence for a Second Graviceptive System in Humans. Neurology. 2000;55:1298-1304
    ↑卡恩霍 HO, 費伯 S, 柴可斯 J. 推車行為的起源：人類第二個重力感受系統的證據. 神經學. 2000;55:1298-1304
  20. ↑ Jump up to: 20.0 20.1 20.2 Bergmann J, Krewer C, Rieß K, Müller F, Koenig E, Jahn K. Inconsistent classification of pusher behaviour in stroke patients: A direct comparison of the Scale for Contraversive Pushing and the Burke Lateropulsion Scale. Clinical rehabilitation. 2014 Jan 23:0269215513517726.
    ↑ Jump up to: 20.0 20.1 20.2 諾貝曼 J, 克魯埃 C, 梅斯 K, 慕勒 F, 邸格 E, 甘恩 K. 腎中風患者推車行為的一致分類：直接比較 Scale for Contraversive Pushing 與 Burke Lateropulsion Scale. 临床復康. 2014 年 1 月 23 日:0269215513517726.
  21. ↑ Karnath H-O, Ferber S, Dichgans J. The neural representation of postural control in humans. Proc Natl Acad Sci U S A.2000 ;97:13931–13936.
    ↑Karnath H-O, Ferber S, Dichgans J. 人類姿勢控制的神經表徵。美國國家科學院院刊。2000 ;97:13931–13936.
  22. ↑ Yang YR, Chen YH, Chang HC, Chan RC, Wei SH, Wang RY. Effects of interactive visual feedback training on post-stroke pusher syndrome: a pilot randomized controlled study. Clinical rehabilitation. 2015 Oct;29(10):987-93.
    ↑楊 YR, 陳 YH, 舒安 HC, 陳 RC, 魏 SH, 王 RY. 交互視覺回饋訓練對中風後推車症候群的影響：一項初步隨機對照研究. 临床康复. 2015 10;29(10):987-93.
  23. ↑ Romick-Sheldon D, Kimalat A. Novel treatment approach to contraversive pushing after acute stroke: A case report. Physiotherapy Canada. 2017;69(4):313-7.
    ↑羅米克-謝倫 D, 克米拉特 A. 急性中風後對側推進的新治療方法：一例報告. 物理治療加拿大. 2017;69(4):313-7.
  24. ↑ Bergmann J, Krewer C, Jahn K, Müller F. Robot-assisted gait training to reduce pusher behavior: A randomized controlled trial. Neurology. 2018 Oct 2;91(14):e1319-27.
    ↑Bergmann J, Krewer C, Jahn K, Müller F. 以機器人輔助步態訓練來減少推物行為：一項隨機對照試驗。神經學。2018 年 10 月 2 日；91(14):e1319-27。
  25. ↑ Gillespie J, Callender L, Driver S. Usefulness of a standing frame to improve contraversive pushing in a patient post-stroke in inpatient rehabilitation. InBaylor University Medical Center Proceedings 2019 Jul 3 (Vol. 32, No. 3, pp. 440-442). Taylor & Francis.
    ↑吉爾斯比 J, 喬利安 L, 德韋爾 S. 在中風後入院康復患者中使用站立架改善對側推進的有用性. 《貝勒大學醫學院 proceedings》2019 年 7 月 3 日 (第 32 卷, 第 3 期, 頁 440-442). 派爾弗里森.
  26. ↑ ARC Seminars L.L.C. Pusher Syndrome: How to better facilitate midline orientation. Available from: https://www.youtube.com/watch?v=0zfJBwuNAHc [Accessed, 17/09/2021]
    ↑ARC 塞米納斯 L.L.C. 推動綜合症：如何更好地促進中線定向. 可從: https://www.youtube.com/watch?v=0zfJBwuNAHc [於 2021 年 9 月 17 日訪問]
  27. ↑ Karnath HO. Pusher syndrome–a frequent but little-known disturbance of body orientation perception. Journal of neurology. 2007 Apr;254:415-24.
    ↑卡恩霍. 推動綜合症—一種常見但少為人知的身體定向知覺障礙. 神經病學雜誌. 2007 年 4 月;254:415-24.
  28. ↑ van de Rakt J, Mccarthy-Grunwald S. The" Pusher" syndrome, assessment and treatment: part 1. Italian Journal of Sports Rehabilitation and Posturology. 2021;8(18):1904-34.
    ↑范德拉克 J, McCarthy-Grunwald S. "推手"綜合症，評估和治療：第一部分. 意大利運動康復與姿勢學雜誌. 2021;8(18):1904-34.
  29. ↑ van de Rakt J, McCarthy-Grunwald S. The “Pusher “syndrome, assessment and treatment. Part 2. Ita. J. Sports Reh. Po. 2022;9(21):3.
    ↑van de Rakt J, McCarthy-Grunwald S. "推手"症候群，評估與治療。第二部分。義大利運動復健雜誌。2022;9(21):3.


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