Apperceptive agnosia

Last updated

Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. [1] When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; this occurs because apperceptive agnosia is most likely to present visual impairments. [2] However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas. [3]

Contents

Auditory apperceptive agnosia

Auditory apperceptive agnosia are impairments in audition that take place despite intact audiogram. [4] In some cases the deficit is in the ability to recognize spoken words, and in other cases, may be a deficit in recognizing environmental sounds. [4] In all cases individuals are able to read, write, name objects, and converse intelligently. Similar to visual impairments, the deficit arise because of damage in the primary sensory cortex. [4] In the case of auditory agnosia, lesions are present in the superior temporal gyrus bilaterally or in the posterior temporal lobe of the language-dominant (typically left) hemisphere. [4]

In addition to verbal and nonverbal auditory agnosia, there are cases of auditory apperceptive agnosia where patients are unable to recognize music in the absence of sensory, intellectual, and verbal impairments. [5] In these cases there may be a melodic or a memory basis established in the brain and damage to those areas lead to music agnosia.[ citation needed ] Agnosia occurs because of failure to re-encode melodic information properly. This tends to be associated with right-sided lesions interrupting the melodic route in the brain. [5]

Tactile apperceptive agnosia

Tactile apperceptive agnosia results in the inability to shape representations specific to tactile modality.[ citation needed ] The impairment is restricted to the hands even though sensation is not impaired. This is similar to visual apperceptive agnosia in that it is a basic level of processing that is impaired. [6] Some individuals are unable to recognize objects by touch because of a small cerebral infarction. [6] Tactile Apperceptive Agnosia can also affect blind people. A seventy-three year old woman, who was blind since she was born, had been 17 days post coronary bypass grafting, when she started to present some concerns related to her ability to read Braille properly, after being able to read it proficiently from the age of seven. After the surgery, her reading speed was reduced by 75–80%. She was diagnosed with Braille alexia, a rare form of Tactile Apperceptive Agnosia, three months after her surgery, which effects the ability to join to gather tactile stimuli and the processing of that information. Braille reading speed can be affected by this condition, being slowed down due to the reduced pace of processing tactile information. [7]

Olfactory Agnosia

Olfactory agnosia is when a patient can smell something, but they can't identify what the smell is. Like other forms of agnosia, this neural olfactory loss can be due to brain damage, or various diseases like Alzheimer's and Parkinson's disease. [8]

Visual apperceptive agnosia

Visual apperceptive agnosia is a visual impairment that results in a patient's inability to name objects. [9] While agnosics suffer from severe deficits, patients' visual acuity and other visual abilities such as perceiving parts and colours remain intact. [6] Deficits seem to occur because of damage to early-level perceptual processing. [9] While patients are able to effectively allocate attention to locate the object and perceive the parts, they are unable to group together the parts they see and name the object accurately. [10] This is demonstrated by the fact that patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch. [2]

Origin

Following Hermann Munk's identification of a condition he called "Seelenblindheit" (mind-blindness) Heinrich Lissauer published an exhaustive diagnostic evaluation of a patient who could not, or only with great difficulty, visually identify common objects. [11] Because primary visual processing was intact, Lissauer considered the possible diagnostic distinction between deficits in perception (apperceptive agnosia) and in recognition (associative agnosia).[ citation needed ]

The topic became prominent when Kurt Goldstein and Adhėmar Gelb published performance details of a patient Schn. with shrapnel fragments in the brain, the result of being wounded in World War I. . [12] He was followed over many years and created a great deal of controversy when subsequent tests were found to be at variance with the original findings. [13]

Effects

Apperceptive visual agnosia results in profound difficulties on a patient's ability to recognize visually presented information. [14] Apperceptive agnosia affects the perceptual processing of individuals. Impairments of elements such as color and motion makes it difficult to interpret shape or the spatial arrangements of objects. [15] Deficits in apperceptive agnosics have not been linked to deficits in acuity. Additionally, patients have an intact ability to attend to cued stimuli. [10] They have the ability to maintain fixation, reach for moving targets, and write as well. Those with apperceptive agnosia, however, have difficulty copying geometric shapes and letters. In some cases individuals are able to trace letters and shapes with their finger but they are unable to use the technique as a strategy to name objects. [14]

Deficits in apperceptive agnosics seem to be differential based on categories.[ citation needed ] Apperceptive agnosia has been noted to affect both broad and specific deficits[ citation needed ]. Specific deficits include impairments in the recognition of body parts, buildings, manipulated objects, animals, and places. [9] Picture naming is impaired in visual apperceptive agnosia but recognition of objects can be achieved through accessing other modalities. For example, an object can be recognized through touch. [6] Also when it is spoken about, individuals with apperceptive agnosia are able to define the object. [16] The continuing of the ability of patients to recognize the object through use of different sensory modalities shows that deficits arise because of a breakdown in the interaction between visual systems and semantic memory. [16]

Location of brain damage

Each patient that suffers from apperceptive agnosia does not have brain damage in exactly the same area. However, brain damage in proximity to the occipital lobe is largely correlated with the patterns of deficit seen in apperceptive agnostics. [2] For example, patient JB suffered extensive damage to the parietal-occipital areas to the left cerebral hemisphere leading to his deficit in the ability to name distinguish between structurally similar object. [16]

Visually presented object recognition is largely mediated by a hierarchical occipitotemporal pathway. [17] This pathway facilitates the distinction between regions allowing the processing of the visual features of objects. In addition the occipitoparietal pathway is sometimes damaged in apperceptive agnosia patients.[ citation needed ] Damage to this region leads to impairments in localization of visual stimuli. [17]

Theories of causation

No two apperceptive agnosic patients are the same, but case studies have been used to make theories on what causes the object recognition deficits.[ citation needed ] While it is established that semantics plays a large role in apperceptive agnosia deficits, it is not agreed upon how semantics alter recognition processes. [ citation needed ]One theory proposes that semantic memories are divided into differential semantic categories. Brain damage leads to apperceptive agnosia because there is damage to a particular semantic category.[ citation needed ] Another theory, referred to as functional specialization, states that individual parts of the brain specialize in different tasks. According to this theory, if an area of the brain is damaged, the function that the area is responsible for may decline as well. Yet another theory suggests that the pattern of deficit arise from independent impairments to a particular input modality and a single non perceptual semantic system that is organized by category.[ citation needed ] Deficits are largely due to semantics, however many categories are related perceptually as well. [18] Objects that are biologically similar are likely to have physical resemblance to each other as well.[ citation needed ] Evidence for this arises in the finding that perceptual confusion arises because of structural similarity contributes or accounts for some modality specific deficit. [14]

Object processing is said to occur by two processes.[ citation needed ] There is first a stage of object perception.[ citation needed ] In this step there is mapping of visual description from the stimulus to a set of stored structural descriptions onto a set of structural descriptions of familiar objects. [14] In the second stage, there is object identification.[ citation needed ] In this step the structural description is mapped onto the semantic representations giving rise to a full specification of the object. [18] Researchers differ in their belief [ citation needed ] of how perceptual knowledge has an effect. Some believe that the loss of perceptual attributes should always accompany structural similarity. Others observe that perceptual and structural information often accompany each other but they believe that the information can occur independently from each other. Based on patient information it seems that objects belonging to a category with many structurally similar neighbours would be vulnerable to this semantic access impairment. [16]

Case studies

No two apperceptive agnosics are the same so it is beneficial to look at individuals who suffer from apperceptive agnosia to see the range of impairments that can occur and the range of functioning that can remain.[ citation needed ]

JB

Patient JB was able to match spoken words to target pictures almost perfectly when the target was presented with three other dissimilar distractors from the same semantic category. However, when the distractors were similar to each other and from the same semantic category his functioning decreased significantly. His abilities show evidence that the problem may lie in an interaction between processes involved in specification of the object's visual structural description and access to semantic systems. [16]

ELM

Patient ELM was sixty-one years old when this case study was under review. In 1982, he was first admitted to a hospital for Atrial Fibrillation, and presented symptoms of left/ right confusion, nominal dysphasia, agraphia (minus the Alexia), and dysgraphia. After further examination, it was discovered that ELM had a Cortical Lesion in his left hemisphere in the temporal lobe. [19] ELM has deficits in the ability to name drawings of living things even though her ability to name man-made things remain intact. The early visual processing of shapes appear to be intact as well. In addition, unlike many patients, the ability to identify overlapping drawings of man-made objects remained intact. ELM was able to match both living and non-living things viewed from different perspectives. ELM's deficit lied in the fact that she was not able to distinguish between drawings that were real and plausibly unreal objects that were living; however, she was able to make the distinction when the objects were man made. Her impairments resulted due to damage to structural description of living things. There were problems with integrating features of structurally similar shapes of objects belonging to the same semantic category. This inability might be because of the distance between associated objects. The ones that are semantically close to each other are harder to differentiate. [16]

HJA

HJA had deficits in differentiating between living things. She also made errors while naming line drawings. Instead of naming the pictures HJA frequently gave feature-by-feature description of the object (e.g. instead of saying circle, she would say many little dots). In addition, she would separate parts of drawn object instead of saying the name of the whole (e.g. handle and hairs when referring to paintbrush). HJA has problems segmenting global shapes when elements are closely grouped together. However, unlike the other patients, HJA has no problem copying and identifying overlapping drawings. In addition, HJA was able to draw objects accurately from the memory. [16]

Populations affected

There are subsets of groups in which apperceptive agnosia is more widespread.[ citation needed ]

Alzheimer's disease

Visual agnosia (both apperceptive and associative) is prevalent in Alzheimer's disease (AD) patients. Visual agnosia may be present in early stages of AD and can often act as an indicator of AD. [20] Apperceptive agnosia results from diffuse cortical pathology of AD. There is early involvement in the hippocampus and the entorhinal cortex followed by a spread to adjacent areas with neurofibrillary tangles (NFT). Gradual extension of NFT throughout the occipital, parietal, and temporal regions devoted to vision occur resulting in visual agnosia. [15]

See also

Related Research Articles

<span class="mw-page-title-main">Agnosia</span> Medical condition

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

<span class="mw-page-title-main">Prosopagnosia</span> Cognitive disorder of face perception

Prosopagnosia, also known as face blindness, is a cognitive disorder of face perception in which the ability to recognize familiar faces, including one's own face (self-recognition), is impaired, while other aspects of visual processing and intellectual functioning remain intact. The term originally referred to a condition following acute brain damage, but a congenital or developmental form of the disorder also exists, with a prevalence of 2.5%. The brain area usually associated with prosopagnosia is the fusiform gyrus, which activates specifically in response to faces. The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. For those with prosopagnosia, the method for recognizing faces depends on the less sensitive object-recognition system. The right hemisphere fusiform gyrus is more often involved in familiar face recognition than the left. It remains unclear whether the fusiform gyrus is specific for the recognition of human faces or if it is also involved in highly trained visual stimuli.

Semantic memory refers to general world knowledge that humans have accumulated throughout their lives. This general knowledge is intertwined in experience and dependent on culture. New concepts are learned by applying knowledge learned from things in the past.

Astereognosis is the inability to identify an object by active touch of the hands without other sensory input, such as visual or sensory information. An individual with astereognosis is unable to identify objects by handling them, despite intact elementary tactile, proprioceptive, and thermal sensation. With the absence of vision, an individual with astereognosis is unable to identify what is placed in their hand based on cues such as texture, size, spatial properties, and temperature. As opposed to agnosia, when the object is observed visually, one should be able to successfully identify the object.

Simultanagnosia is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation. The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

<span class="mw-page-title-main">Associative visual agnosia</span> Medical condition

Associative visual agnosia is a form of visual agnosia. It is an impairment in recognition or assigning meaning to a stimulus that is accurately perceived and not associated with a generalized deficit in intelligence, memory, language or attention. The disorder appears to be very uncommon in a "pure" or uncomplicated form and is usually accompanied by other complex neuropsychological problems due to the nature of the etiology. Affected individuals can accurately distinguish the object, as demonstrated by the ability to draw a picture of it or categorize accurately, yet they are unable to identify the object, its features or its functions.

Semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain. Semantic dementia is a disorder of semantic memory that causes patients to lose the ability to match words or images to their meanings. However, it is fairly rare for patients with semantic dementia to develop category specific impairments, though there have been documented cases of it occurring. Typically, a more generalized semantic impairment results from dimmed semantic representations in the brain.

Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision, language, memory, or intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain.[2] There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

Auditory verbal agnosia (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients.

Akinetopsia, also known as cerebral akinetopsia or motion blindness, is a term introduced by Semir Zeki to describe an extremely rare neuropsychological disorder, having only been documented in a handful of medical cases, in which a patient cannot perceive motion in their visual field, despite being able to see stationary objects without issue. The syndrome is the result of damage to visual area V5, whose cells are specialized to detect directional visual motion. There are varying degrees of akinetopsia: from seeing motion as frames of a cinema reel to an inability to discriminate any motion. There is currently no effective treatment or cure for akinetopsia.

Autotopagnosia from the Greek a and gnosis, meaning "without knowledge", topos meaning "place", and auto meaning "oneself", autotopagnosia virtually translates to the "lack of knowledge about one's own space," and is clinically described as such.

<span class="mw-page-title-main">Integrative agnosia</span> Medical condition

Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which determines the specificity of the disease being Integrative. This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to integrate parts such as spatial distances or producing visual images from short or long-term memory.

Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. While auditory agnosia impairs the understanding of sounds, other abilities such as reading, writing, and speaking are not hindered. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway.

Extinction is a neurological disorder that impairs the ability to perceive multiple stimuli of the same type simultaneously. Extinction is usually caused by damage resulting in lesions on one side of the brain. Those who are affected by extinction have a lack of awareness in the contralesional side of space and a loss of exploratory search and other actions normally directed toward that side.

Visual object recognition refers to the ability to identify the objects in view based on visual input. One important signature of visual object recognition is "object invariance", or the ability to identify objects across changes in the detailed context in which objects are viewed, including changes in illumination, object pose, and background context.

Phonagnosia is a type of agnosia, or loss of knowledge, that involves a disturbance in the recognition of familiar voices and the impairment of voice discrimination abilities in which the affected individual does not suffer from comprehension deficits. Phonagnosia is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage, other auditory agnosias include cortical deafness and auditory verbal agnosia also known as pure word deafness.

Topographical disorientation is the inability to orient oneself in one's surroundings, sometimes as a result of focal brain damage. This disability may result from the inability to make use of selective spatial information or to orient by means of specific cognitive strategies such as the ability to form a mental representation of the environment, also known as a cognitive map. It may be part of a syndrome known as visuospatial dysgnosia.

Form perception is the recognition of visual elements of objects, specifically those to do with shapes, patterns and previously identified important characteristics. An object is perceived by the retina as a two-dimensional image, but the image can vary for the same object in terms of the context with which it is viewed, the apparent size of the object, the angle from which it is viewed, how illuminated it is, as well as where it resides in the field of vision. Despite the fact that each instance of observing an object leads to a unique retinal response pattern, the visual processing in the brain is capable of recognizing these experiences as analogous, allowing invariant object recognition. Visual processing occurs in a hierarchy with the lowest levels recognizing lines and contours, and slightly higher levels performing tasks such as completing boundaries and recognizing contour combinations. The highest levels integrate the perceived information to recognize an entire object. Essentially object recognition is the ability to assign labels to objects in order to categorize and identify them, thus distinguishing one object from another. During visual processing information is not created, but rather reformatted in a way that draws out the most detailed information of the stimulus.

Patient DF is a woman with visual apperceptive agnosia who has been studied extensively due to the implications of her behavior for the two streams theory of visual perception. Though her vision remains intact, she has trouble visually locating and identifying objects. Her agnosia is thought to be caused by a bilateral lesion to her lateral occipital cortex, an area thought by dual-stream proponents to be the ventral "object recognition" stream. Despite being unable to identify or recognize objects, DF can still use visual input to guide her action.

References

  1. ↑ David Andrewes (13 May 2013). Neuropsychology: From Theory to Practice. Psychology Press. p. 50. ISBN   978-1-134-95046-1.
  2. 1 2 3 Shelton, P.A.; Bowers, D.; Duara, R. (1994). "Apperceptive Visual Agnosia: A Case Study". Brain and Cognition. 25 (1): 1–23. doi: 10.1006/brcg.1994.1019 . PMID   8043261. S2CID   30261660.
  3. ↑ De Renzi, E. (2000). "Disorder of Visual Recognition". Seminars in Neurology. 20 (4): 479–485. doi:10.1055/s-2000-13181. PMID   11149704.
  4. 1 2 3 4 Buchtel, H.A.; Stewart, J.D. (1989). "Auditory Agnosia: Apperceptive or Associative Disorder?". Brain and Language. 37 (1): 12–25. doi:10.1016/0093-934X(89)90098-9. PMID   2752270. S2CID   7549010.
  5. 1 2 Ayotte, J.; Peretz, I.; Rousseau, I.; Bard, C.; Bojanowski, M. (2000). "Patterns of Music Agnosia Associated with Middle Cerebral Artery Infarcts". Brain. 123 (9): 1926–1938. doi: 10.1093/brain/123.9.1926 . PMID   10960056.
  6. 1 2 3 4 Reed, C.L.; Caselli, R.J.; Farah, M.J. (1996). "Tactile Agnosia - Underlying Impairment and Implications for Normal Tactile Object Recognition". Brain. 119 (3): 875–888. doi:10.1093/brain/119.3.875. PMID   8673499.
  7. ↑ Larner, Andrew J (August 2007). "Braille alexia: an apperceptive tactile agnosia?". Journal of Neurology, Neurosurgery, and Psychiatry. 78 (8): 907–908. doi:10.1136/jnnp.2006.106922. ISSN   0022-3050. PMC   2117751 . PMID   17635985.
  8. ↑ Lalwani, Anil K. (2012), Lalwani, Anil K. (ed.), "Chapter 10. Olfactory Dysfunction", CURRENT Diagnosis & Treatment in Otolaryngology—Head & Neck Surgery (3 ed.), New York, NY: The McGraw-Hill Companies, retrieved 2020-07-01
  9. 1 2 3 Vecera, S.; Gilds, K. (1998). "What Processing Is Impaired in Apperceptive Agnosia? Evidence from Normal Subjects". Journal of Cognitive Neuroscience. 10 (5): 568–80. doi:10.1162/089892998562979. PMID   9802990. S2CID   21568462.
  10. 1 2 Abrams, R.A.; Law, M.B (2002). "Random Visual Noise Impairs Object-based Attention". Exp Brain Res. 142 (3): 349–353. doi:10.1007/s00221-001-0899-2. PMID   11819043. S2CID   10236264.
  11. ↑ Lissauer H (1890). "Ein Fall von Seelenblindheit". Archiv für Psychiatrie und Nervenkrankheiten. 21 (2): 222–270. doi:10.1007/bf02226765. S2CID   29786214.
  12. ↑ Gelb, A, Goldstein, K (1920) Zur Psychologie des optischen Wahrnehmungs und Erkennungsvorgangs.pp 1- 142 In Psychologische Analysen hirnpatholosicher Fälle. Leipzig: J.A. Barth
  13. ↑ Jung R (1949). "Uber eine Nachuntersuchung des Falles Schn. von Goldstein und Gelb". Psychiatrie Neurologie und Medizinische Psychologie. 1: 353–362.
  14. 1 2 3 4 Grossman, M.; Galetta, S.; D'esposito, M. (1997). "Object Recognition Difficulty in Visual Apperceptive Agnosia". Brain and Cognition. 33 (3): 306–342. doi: 10.1006/brcg.1997.0876 . PMID   9126398. S2CID   11582998.
  15. 1 2 Duffy CJ (January 1999). "Visual loss in Alzheimer's disease: out of sight, out of mind". Neurology. 52 (1): 10–1. doi:10.1212/wnl.52.1.10. PMID   9921840. S2CID   45432450.
  16. 1 2 3 4 5 6 7 Funnell, E. (2000). "Apperceptive Agnosia and the Visual Recognition of Object Categories in Dementia of the Alzheimer Type". Neurocase. 6 (6): 451–463. doi:10.1080/13554790008402716. S2CID   144011405.
  17. 1 2 Ferreira, C.T.; Ceccaldi, M; Giusiano, B.; Poncet, M. (1998). "Separate Visual Pathways for Perception of Actions and Objects: Evidence from A Case Apperceptive Agnosia". J Neurol Neurosurg Psychiatryiatry. 65 (3): 382–385. doi:10.1136/jnnp.65.3.382. PMC   2170224 . PMID   9728957.
  18. 1 2 De Renzi E (2000). "Disorder of Visual Recognition". Seminars in Neurology. 20 (4): 479–485. doi:10.1055/s-2000-13181. PMID   11149704.
  19. ↑ Forde, Emer; Humphreys, Glyn (2005-07-22). Category Specificity in Brain and Mind. Psychology Press. ISBN   978-1-135-42625-5.
  20. ↑ Giannakopoulos, P.; Gold, G.; Duc, M.; Michel, J.-P.; Hof, P.R; Bouras, C. (1999). "Neuroanatomic Correlates of Visual Agnosia in Alzheimer's Disease: A Clinicopathologic". Neurology. 52 (1): 71–77. doi:10.1212/wnl.52.1.71. PMID   9921851. S2CID   25961742 . Retrieved 10 March 2012.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.