Feroze Kaberi B., Gurnani Bharat, O'Rourke Maria C.
King Faisal University
Gomabai Netralaya and Research Centre
Transient vision loss (TVL) is an ophthalmological symptom that instills apprehension in the minds of patients and clinicians. The patient is usually concerned that the loss is permanent, while the clinician focuses on ruling out severe underlying pathology. Causes vary and include life-threatening conditions such as carotid artery disease or cardiac emboli. Alternatively, a benign migraine can also cause transient vision loss. Appropriate assessment of patients presenting with this symptom is necessary to address the underlying cause adequately. TVL is a temporary and sudden loss of visual acuity in 1 or both eyes. When multiple vision fields are affected, they may be called transient visual obscurations (TVOs). This condition can be alarming for patients and presents a diagnostic challenge for clinicians. Understanding the potential etiologies, associated anatomy, natural history, and spread patterns is crucial for effective diagnosis and management. Transient vision loss can occur in various clinical scenarios and is often a symptom of underlying systemic or ocular conditions. The duration of vision loss typically ranges from a few seconds to minutes and may occur intermittently. TVOs are often described as a gray or black curtain descending over the visual image and are sometimes accompanied by flashes of light (photopsia) or geometric shapes (scintillating scotomas). Transient vision loss can result from any disruption along the visual pathway. The following structures may be disrupted: The retina receives and processes light, converting it into neural signals. The macula of the retina plays a critical role in central vision. The central retinal artery, vein, and optic nerve head are essential for maintaining retinal function. This cranial nerve (CN II) transmits visual information from the retina to the brain and is susceptible to ischemia, inflammation, and compression. The optic nerves partially cross here, forming optic tracts that convey information to the thalamus's lateral geniculate nucleus (LGN). Located in the thalamus, the LGN processes and relays visual information to the visual cortex. The primary visual cortex (V1) interprets the visual information received in the occipital lobe. Common causes of transient vision loss may be grouped based on system or mechanism: Transient ischemic attacks (TIAs) affecting the ocular circulation, such as amaurosis fugax. These events are often harbingers of more severe cerebrovascular accidents (strokes). Conditions like giant cell arteritis (GCA), papilledema, and optic neuritis can lead to transient vision loss. GCA, an inflammatory condition affecting medium and large arteries, can cause severe visual impairment if untreated. Papilledema, caused by increased intracranial pressure, leads to transient obscuration due to optic nerve head swelling. Migraine with aura, characterized by visual disturbances preceding headache, is often accompanied by transient vision loss. Seizures and other cortical events can also produce transient visual symptoms. Transient vision loss can occur due to mechanical pressure on the optic nerve or globe, as seen in certain head positions or during Valsalva maneuvers. Transient vision loss can have various presentations based on multiple features: Monocular vision loss suggests disruption anterior to the optic chiasm (ie, retina or optic nerve), while binocular loss typically results from post-chiasmal pathology (ie, optic tracts, LGN, or visual cortex). Short, repetitive episodes typically indicate a vascular or mechanical cause, while longer durations are associated with inflammatory or demyelinating diseases. The presence of pain (eg, optic neuritis), headache (eg, migraines), or systemic symptoms (eg, jaw claudication in GCA) can guide the differential diagnosis. Early identification and treatment of the underlying causes are essential to prevent permanent visual loss and associated morbidity. Transient vision loss is a concerning symptom requiring a thorough evaluation to rule out potentially life-threatening conditions.
短暂性视力丧失(TVL)是一种眼科症状,会使患者和临床医生感到担忧。患者通常担心视力丧失是永久性的,而临床医生则专注于排除严重的潜在病变。病因多种多样,包括危及生命的疾病,如颈动脉疾病或心脏栓子。另外,良性偏头痛也可导致短暂性视力丧失。对出现此症状的患者进行适当评估,对于充分解决潜在病因至关重要。短暂性视力丧失是一只或两只眼睛视力的暂时突然丧失。当多个视野受到影响时,它们可能被称为短暂性视觉模糊(TVO)。这种情况可能会让患者感到恐慌,并给临床医生带来诊断挑战。了解潜在病因、相关解剖结构、自然病史和扩散模式对于有效诊断和管理至关重要。短暂性视力丧失可发生在各种临床情况下,通常是潜在全身性或眼部疾病的症状。视力丧失的持续时间通常从几秒到几分钟不等,可能间歇性发生。短暂性视觉模糊通常被描述为一道灰色或黑色的幕布降临在视觉图像上,有时还伴有闪光(光幻视)或几何形状(闪烁暗点)。短暂性视力丧失可由视觉通路中的任何干扰引起。以下结构可能受到干扰:视网膜接收并处理光线,将其转化为神经信号。视网膜黄斑在中心视力中起关键作用。视网膜中央动脉、静脉和视神经乳头对于维持视网膜功能至关重要。这条脑神经(CN II)将视觉信息从视网膜传递到大脑,易受缺血、炎症和压迫影响。视神经在此处部分交叉,形成视束,将信息传递到丘脑的外侧膝状体核(LGN)。位于丘脑的外侧膝状体核处理视觉信息并将其传递到视觉皮层。初级视觉皮层(V1)解释在枕叶接收到的视觉信息。短暂性视力丧失的常见病因可根据系统或机制进行分类:影响眼部循环的短暂性脑缺血发作(TIA),如一过性黑矇。这些事件往往是更严重脑血管意外(中风)的先兆。巨细胞动脉炎(GCA)、视乳头水肿和视神经炎等疾病可导致短暂性视力丧失。巨细胞动脉炎是一种影响中大型动脉的炎症性疾病,若不治疗可导致严重视力损害。视乳头水肿由颅内压升高引起,由于视神经乳头肿胀导致短暂性模糊。伴有先兆的偏头痛,其特征为头痛前出现视觉障碍,常伴有短暂性视力丧失。癫痫发作和其他皮层事件也可产生短暂性视觉症状。短暂性视力丧失可由于对视神经或眼球的机械压迫而发生,如在某些头部位置或瓦尔萨尔瓦动作期间所见。基于多种特征,短暂性视力丧失可有多种表现:单眼视力丧失提示视交叉前方(即视网膜或视神经)出现干扰,而双眼视力丧失通常由视交叉后病变(即视束、外侧膝状体核或视觉皮层)引起。短暂、反复的发作通常表明是血管性或机械性原因,而持续时间较长则与炎症性或脱髓鞘疾病有关。疼痛(如视神经炎)、头痛(如偏头痛)或全身症状(如巨细胞动脉炎中的颞颌关节疼痛)的存在可指导鉴别诊断。早期识别和治疗潜在病因对于预防永久性视力丧失和相关发病率至关重要。短暂性视力丧失是一个令人担忧的症状,需要进行全面评估以排除潜在的危及生命的疾病。